2005. Conradson, David and Alan Latham. Transnational urbanism: Attending to everyday practices and mobilities. Journal of Ethnic and Migration Studies 31, no. 2 (2005): 227-233.. Smith, Michael Peter. Transnational urbanism revisited. Journal of Ethnic and Migration Studies 31, no. 2 (2005): 235-244.. Beaverstock, Jonathan V. Transnational elites in the city: British highly-skilled inter-company transferees in New York citys financial district. Journal of Ethnic and Migration Studies 31, no. 2 (2005): 245-268.. Yeoh, Brenda S. A. and Katie Willis. Singaporean and British transmigrants in China and the cultural politics of contact zones Journal of Ethnic and Migration Studies 31, no. 2 (2005): 269-285.. Conradson, David and Alan Latham. Friendship, networks and transnationality in a world city: Antipodean transmigrants in London. Journal of Ethnic and Migration Studies 31, no. 2 (2005): 287-305.. Clarke, Nick. Detailing transnational lives of the middle: British working holiday ...
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The ability of cancer cells to migrate through a complex three-dimensional (3D) environment is a hallmark event of cancer metastasis. Therefore, an in vitro migration assay to evaluate cancer cell migration in a 3D setting is valuable to examine cancer progression. Here, we describe such a simple migration assay in a 3D collagen-fibronectin gel for observing cell morphology and comparing the migration abilities of cancer cells. We describe below how to prepare the collagen-fibronectin gel castings, how to set up time-lapse recording, how to draw single-cell trajectories from movies and extract key parameters that characterize cell motility, such as cell speed, directionality, mean square displacement, and directional persistence. In our set-up, cells are sandwiched in a single plane between two collagen-fibronectin gels. This trick facilitates the analysis of cell tracks, which are for the most part 2D, at least in the beginning, but in a 3D environment. This protocol has been previously published in
Given the foolish consistency that comes with being the hobgoblin of little minds, there was no chance that our big-brained president would be consistent on the issue of chain migration. In November, President Donald Trump decried the practice of immigrants sponsoring other family members for permanent residency: CHAIN MIGRATION must end now! Some people come in, and they bring their whole family with them, who can be truly evil. NOT ACCEPTABLE! When the White House released its proposed framework for immigration reform in January, the presidents sentiments were clear: In the future, immigrants would be able to sponsor only spouses and minor children for permanent residency. No more parents or siblings. But the presidents distaste for chain migration apparently doesnt apply to his extended family.. On Thursday, the presidents in-laws, Amalija and Viktor Knavs, became naturalized U.S. citizens, thanks to the sponsorship of their immigrant daughter, first lady Melania Trump. Good for ...
We first examined the effect of afadin on cell movement in response to PDGF stimulation using wild-type and afadin-knockdown NIH3T3 cells. The expression level of afadin in both cell types is shown in Fig. 1A. Wild-type and afadin-knockdown NIH3T3 cells were sparsely plated on μ-Slide VI Flow dishes pre-coated with vitronectin, an extracellular matrix protein that binds to αvβ3 integrin (Schvartz et al., 1999), and were directionally stimulated with PDGF. Wild-type NIH3T3 cells became polarized with the well-spreading leading edge toward the higher concentration of PDGF, whereas afadin-knockdown NIH3T3 cells showed elongated shapes and had a small leading edge that was randomly directed and was independent of the direction of the higher concentration of PDGF (Fig. 1B).. These results led us to assume that afadin is involved in directional cell movement. To examine this assumption, we performed a wound-healing assay by scratching the confluent monolayer of wild-type and afadin-knockdown NIH3T3 ...
Since MMP activity is also regulated by TIMP binding (Nagase and Woessner, 1999) and the dissociation of TIMP-MMP complexes during gel electrophoresis prior to zymography assays acts to enhance the apparent activity of proMMP isoforms, soluble gelatinase activity in the cell‐conditioned media samples was assayed using a peptide substrate (Figure 6C). Both v‐Src3T3 and v‐Src FRNK S‐1034 cells contained high levels of soluble gelatinase activity, whereas NIH‐3T3 and the various v‐Src FRNK cell clones had ∼4‐fold lower levels of gelatinase activity secreted from the same number of cells (Figure 6C). Analysis of whole‐cell lysates also revealed that FRNK expression resulted in lower levels of cell‐associated gelatinase activity (Figure 6D). Although blotting analyses did not reveal significant changes in TIMP expression (data not shown), addition of recombinant TIMP‐2 to v‐Src3T3s inhibited Matrigel invasion activity in a dose‐dependent manner (Figure 6E). Taken together, ...
Proliferation and tangential migration of neural precursor cells are essential determinants of CNS development. We have established cell culture models of both these processes using neural precursor cells grown as neurospheres. The pattern of migration that we observe in these cells is homotypic and occurs in the absence of a glial or neuronal scaffold, and is therefore equivalent to that previously described as chain migration. To determine the role of integrins in proliferation and migration, we have analysed the expression pattern of integrins on neurosphere cells and then performed blocking peptide and antibody experiments. Neurosphere cells express five major integrins, alpha5 beta1, alpha 6Abeta1, alphav beta1, alphav beta5 and alpha vbeta8 and, in addition, express low levels of alpha 6Bbeta1. Chain migration is inhibited by blocking the alpha 6beta1 integrin. Proliferation, by contrast, is inhibited by blocking the other beta1 integrins, alphav beta1 and alpha5 beta1. These results show ...
BACKGROUND AND PURPOSE: Vascular smooth muscle cell (SMC) migration within the arterial wall is a crucial event in atherogenesis and restenosis. Monocyte chemotactic protein-1/CC-chemokine receptor 2 (MCP-1/CCR2) signalling is involved in SMC migration processes but the molecular mechanisms have not been well characterized. We investigated the role of PI3Kγ in SMC migration induced by MCP-1. EXPERIMENTAL APPROACHES: A pharmacological PI3Kγ inhibitor, adenovirus encoding inactive forms of PI3Kγ and genetic deletion of PI3Kγ were used to investigate PI3Kγ functions in the MCP-1 and platelet-derived growth factor (PDGF) signalling pathway and migration process in primary aortic SMC. KEY RESULTS: The γ isoform of PI3K was shown to be the major signalling molecule mediating PKB phosphorylation in MCP-1-stimulated SMC. Using a PI3Kγ inhibitor and an adenovirus encoding a dominant negative form of PI3Kγ, we demonstrated that PI3Kγ is essential for SMC migration triggered by MCP-1. PDGF receptor
A broad range of biological processes such as morphogenesis, tissue regeneration, and cancer invasion depend on the collective migration of epithelial cells. Guidance of collective cell migration is commonly attributed to soluble or immobilized chemical gradients. I will present novel mechanisms of collective cellular guidance that are physical in origin rather than chemical. Firstly, I will focus on how the mechanical interaction between the tumor and its stroma guides cancer cell invasion. I will show that cancer associated fibroblasts exert a physical force on cancer cells that enables their collective invasion. In the second part of my talk I will focus on durotaxis, the ability of cells to follow gradients of extracellular matrix stiffness. Durotaxis is well established as a single cell phenomenon but whether it can direct the motion of cell collectives is unknown. I will show that durotaxis emerges in cell collectives even if isolated constituent cells are unable to durotax. Collective ...
Marian Blanca Ramírez from the CSIC in Spain has been studying the effects of LRRK2, a protein associated with Parkinsons disease, on cell motility. A Travelling Fellowship from Journal of Cell Science allowed her to spend time in Prof Maddy Parsons lab at Kings College London, learning new cell migration assays and analysing fibroblasts cultured from individuals with Parkinsons. Read more on her story here. Where could your research take you? The deadline to apply for the current round of Travelling Fellowships is 23rd Feburary 2018. Apply now!. ...
An initial step in solid tumor metastasis involves the migration of tumor cells through extracellular matrix. Several cancer cell migration strategies exist in vivo, and the local properties of collagen fibers are implicated in modulating migration behaviors. Yet, individual tumor cells also display heterogeneity in their intrinsic ability to migrate and metastasize. It remains unclear to what extent intrinsic and extrinsic heterogeneity contribute to the emergence of distinct migration phenotypes and whether certain migration phenotypes contribute more to metastasis than others. To study this, we generated 3D collagen matrices of varying densities and monitored single cancer cell migration in these matrices with time-lapse microscopy. We observed a collagen density threshold at 2.5mg/ml, above which 86% of MDA-MB-231 breast cancer cells transition from single mesenchymal migration to collective cell migration, with a 50% increase in persistence after cell division. After seven days, these ...
The migration of T lymphocytes is a vital component of the immune system, with roles in immunosurveillance and inflammation. The role of Phosphoinositide 3-kinase within T lymphocyte migration is unclear, with some evidence that it may be a disposable signal. Here, using Staphylococcal Enterotoxin B activated peripheral blood mononuclear cells and the T cell line CEM cells, the role of Phosphoinositide 3-kinase and its downstream kinases was investigated. CCL22 mediated CEM cell migration and CXCL12 mediated peripheral blood mononuclear cell migration were shown to be independent of Phosphoinositide 3-kinase using several different broad-spectrum Phosphoinositide 3-kinase inhibitors. However, these cells were Akt-dependent, as demonstrated by incubation with the Akt inhibitor Akti-1/2. Differences in the effect of the inhibitors on Akt activity were discovered, indicating that either Akt can be activated in the absence of Phosphoinositide 3-kinase, or differences exist regarding the relative ...
Ilina, Elena I.; Armento, Angela; Sanchez, Leticia Garea; Reichlmeir, Marina; Braun, Yannick; Penski, Cornelia; Capper, David; Sahm, Felix; Jennewein, Lukas; Harter, Patrick N.; Zukunft, Sven; Fleming, Ingrid; Schulte, Dorothea; Le Guerroue, Francois; Behrends, Christian; Ronellenfitsch, Michael W.; Naumann, Ulrike; Mittelbronn, Michel ...
TY - JOUR. T1 - Hydrogen Peroxide Triggers a Dual Signaling Axis To Selectively Suppress Activated Human T Lymphocyte Migration.. AU - Ball, Jennifer. AU - Vlisidou, Isabella. AU - Blunt, Matthew. AU - Wood, William. AU - Ward, Stephen. PY - 2017/5/1. Y1 - 2017/5/1. N2 - H2O2 is an early danger cue required for innate immune cell recruitment to wounds. To date, little is known about whether H2O2 is required for the migration of human adaptive immune cells to sites of inflammation. However, oxidative stress is known to impair T cell activity, induce actin stiffness, and inhibit cell polarization. In this study, we show that low oxidative concentrations of H2O2 also impede chemokinesis and chemotaxis of previously activated human T cells to CXCL11, but not CXCL10 or CXCL12. We show that this deficiency in migration is due to a reduction in inflammatory chemokine receptor CXCR3 surface expression and cellular activation of lipid phosphatase SHIP-1. We demonstrate that H2O2 acts through an Src ...
Cell invasion through extracellular matrix (ECM) is a critical step in tumor metastasis. To study cell invasion in vitro, the internal microenvironment can be simulated via the application of 3D models. This study presents a method for 3D invasion examination using microcarrier-based spheroids. Cell invasiveness can be evaluated by quantifying cell dispersion in matrices or tracking cell movement through time-lapse imaging. It allows measuring of cell invasion and monitoring of dynamic cell behavior in three dimensions. Here we show different invasive capacities of several cell types using this method. The content and concentration of matrices can influence cell invasion, which should be optimized before large scale experiments. We also introduce further analysis methods of this 3D invasion assay, including manual measurements and homemade semi-automatic quantification. Finally, our results indicate that the position of spheroids in a matrix has a strong impact on cell moving paths, which may be easily
The functional integrity of the intestinal epithelial barrier relies on tight coordination of cell proliferation and migration, with failure to regulate these processes resulting in disease. It is not known whether cell proliferation is sufficient to drive epithelial cell migration during homoeostatic turnover of the epithelium. Nor is it known precisely how villus cell migration is affected when proliferation is perturbed. Some reports suggest that proliferation and migration may not be related while other studies support a direct relationship. We used established cell-tracking methods based on thymine analog cell labeling and developed tailored mathematical models to quantify cell proliferation and migration under normal conditions and when proliferation is reduced and when it is temporarily halted. We found that epithelial cell migration velocities along the villi are coupled to cell proliferation rates within the crypts in all conditions. Furthermore, halting and resuming proliferation ...
Collective cell migration is fundamental throughout development, during wound healing and in many diseases. Although much effort has focused on cell-cell junctions, a role for physical confinement in collective cell migration remains unclear. Here, we used adhesive microstripes of varying widths to mimic the spatial confinement experienced by follower cells within epithelial tissues. Our results reveal that the substrate area confinement is sufficient to modulate the three-dimensional cellular morphology without the need for intercellular adhesive cues. Our findings show a direct correlation between the migration velocity of confined cells and their cell-substrate adhesive area. Closer examination revealed that adhesive area confinement reduces lamellipodial protrusive forces, decreases the number of focal complexes at the leading edge and prevents the maturation of focal adhesions at the trailing edge, together leading to less effective forward propelling forces. The release of follower confinement
© 2014 UICC. The ADAMTS proteinases are a family of secreted, matrix-Associated enzymes that have diverse roles in the regulation of tissue organization and vascular homeostasis. Several of the 19 human family members have been identified as having either tumor promoting or suppressing roles. We previously demonstrated that decreased ADAMTS15 expression correlated with a worse clinical outcome in mammary carcinoma (e.g., Porter et al., Int J Cancer 2006;118:1241-7). We have explored the effects of A Disintegrin and Metalloproteinase with Thrombospondin motifs-15 (ADAMTS-15) on the behavior of MDA-MB-231 and MCF-7 breast cancer cells by stable expression of either a wild-type (wt) or metalloproteinase-inactive (E362A) protein. No effects on mammary cancer cell proliferation or apoptosis were observed for either form of ADAMTS-15. However, both forms reduced cell migration on fibronectin or laminin matrices, though motility on a Type I collagen matrix was unimpaired. Knockdown of syndecan-4 attenuated
The ADAMTS proteinases are a family of secreted, matrix-associated enzymes that have diverse roles in the regulation of tissue organization and vascular homeostasis. Several of the 19 human family members have been identified as having either tumor promoting or suppressing roles. We previously demonstrated that decreased ADAMTS15 expression correlated with a worse clinical outcome in mammary carcinoma (e.g., Porter et al., Int J Cancer 2006;118:1241-7). We have explored the effects of A Disintegrin and Metalloproteinase with Thrombospondin motifs-15 (ADAMTS-15) on the behavior of MDA-MB-231 and MCF-7 breast cancer cells by stable expression of either a wild-type (wt) or metalloproteinase-inactive (E362A) protein. No effects on mammary cancer cell proliferation or apoptosis were observed for either form of ADAMTS-15. However, both forms reduced cell migration on fibronectin or laminin matrices, though motility on a Type I collagen matrix was unimpaired. Knockdown of syndecan-4 attenuated the inhibitory
The ADAMTS proteinases are a family of secreted, matrix-associated enzymes that have diverse roles in the regulation of tissue organization and vascular homeostasis. Several of the 19 human family members have been identified as having either tumor promoting or suppressing roles. We previously demonstrated that decreased ADAMTS15 expression correlated with a worse clinical outcome in mammary carcinoma (e.g., Porter et al., Int J Cancer 2006;118:1241-7). We have explored the effects of A Disintegrin and Metalloproteinase with Thrombospondin motifs-15 (ADAMTS-15) on the behavior of MDA-MB-231 and MCF-7 breast cancer cells by stable expression of either a wild-type (wt) or metalloproteinase-inactive (E362A) protein. No effects on mammary cancer cell proliferation or apoptosis were observed for either form of ADAMTS-15. However, both forms reduced cell migration on fibronectin or laminin matrices, though motility on a Type I collagen matrix was unimpaired. Knockdown of syndecan-4 attenuated the inhibitory
How do cells move in a certain direction in the body-go to a wound site and repair it, for example, or hunt down infectious bacteria and kill it?
Cell migration is a highly integrated, multi-step process that plays an important role in the progression of various diseases including cancer, atherosclerosis and arthritis. There are various types and definitions of cell migration. Cell invasion is related to, and encompasses, cell migration, except that cells do more than migrate. Invasive cells move through the extracellular matrix into neighboring tissues in a process that involves ECM degradation and proteolysis. We offer cell migration assays in two formats: Boyden Chamber Assays consist of a cell culture insert nested in the well of cell culture plate. Cells are seeded into the insert and migrate through the pores of the membrane at the bottom of the insert. Gap Closure Assays create a defined area across which cells migrate. Cell migration can be monitored in real time by microscopy. These assays include our new proprietary Radius™ technology which uses a biocompatible hydrogel to create a circular area across which cells can
Cell migration is important in many developmental processes, including neural crest cell migration, gastrulation, and organogenesis. Proper regulation of cell migration is also necessary in adult organisms for immune responses including wound healing. Here, I use the established system of Drosophila border cell migration during oogenesis to provide valuable insight into understanding how collective cell migration is regulated. I have taken a genetic approach to studying cell migration by identifying mutants affecting genes that are important for border cell migration to occur, and a cell biological approach to characterizing the affected cellular behaviors and phenotypes. Through this work, I have mapped novel mutations to genes with previously uncharacterized roles in border cell migration. This analysis has enabled me to describe how Rickets, a G-protein-coupled receptor with a previously unknown role in border cell migration, can coordinate polarity, adhesion, and intercellular communication ...
TY - JOUR. T1 - Arl13b regulates breast cancer cell migration and invasion by controlling integrin-mediated signaling. AU - Casalou, Cristina. AU - Faustino, Alexandra. AU - Silva, Fernanda. AU - Ferreira, Inês C.. AU - Vaqueirinho, Daniela. AU - Ferreira, Andreia. AU - Castanheira, Pedro. AU - Barona, Teresa. AU - Ramalho, José S.. AU - Serpa, Jacinta. AU - Félix, Ana. AU - Barral, Duarte C.. N1 - This work was supported by PhD fellowships from Fundação para a Ciência e a Tecnologia(FCT) to A. Faustino, A. Ferreira and P.C. (PD/BD/105898/2014, PD/BD/135506/2018 and PD/BD/128339/2017, respectively), a post-doctoral fellowship from FCT to C.C. (SFRH/BPD/78561/2011), the FCT Investigator Program to D.C.B. (IF/00501/2014/CP1252/CT0001), and grants from FCT (PTDC/BIM-MEC/4905/2014) and iNOVA4Health - UID/Multi/04462/2013, a program financially supported by FCT/ Ministério da Educação e Ciência, through national funds and co-funded by FEDER under the PT2020 Partnership Agreement.. PY - ...
Cell migration is known to be related to not only physiological phenomena such as embryonic development, immune reaction, and wound healing, but also pathological phenomena such as asthma, vascular disease, and cancer metastasis. However, because genetic mutations of each cancer cell causing high migration ability depend on cell types, it still remains unclear that which pathways are the unity of cancer cell migration signaling irrespective of cancer cell types, and which pathways are the diversity depend on cell types. The aim of this study is to reveal the diversity and unity of regulatory signaling for cancer cell migration based on chemical genomic approach.. To understand the diversity and unity of regulatory signaling for cancer cell migration, the effects of 38 small compounds, whose target protein are already identified, on cell migration ability of 10 types of cancer cells were assessed quantitatively by wound healing assay. Two-way hierarchical clustering was done on migration ability ...
There are numerous biological examples where genes associated with migratory ability of cells also confer the cells with an increased fitness actually though these genes may not really have any known effect about the cell mitosis rates. motility guidelines. We make use of this romantic relationship to make up for motility-induced adjustments in cell size in the CPM therefore that in the fixed CPM, cell size is definitely self-employed of the cell motility. We discover that subject matter to similar amounts of compression, groupings of motile cells develop quicker than groupings of much less motile cells, in qualitative contract with natural findings and our earlier research. Raising compression is likely to decrease development prices. Get in touch with inhibition penalizes clumped cells by halting their development and provides motile cells an actually higher benefit. Finally, our model predicts cell size distributions that are constant with those noticed in groupings of neuroblastoma cells ...
TY - JOUR. T1 - Regulatory T Cell Transmigration and Intravascular Migration Undergo Mechanistically Distinct Regulation at Different Phases of the Inflammatory Response. AU - Snelgrove, Sarah L.. AU - Abeynaike, Latasha D.. AU - Thevalingam, Sukarnan. AU - Deane, James A.. AU - Hickey, Michael J.. PY - 2019/12/1. Y1 - 2019/12/1. N2 - Regulatory T cells (Tregs) play important roles in limiting inflammatory responses in the periphery. During these responses, Treg abundance in affected organs increases and interfering with their recruitment results in exacerbation of inflammation. However, the mechanisms whereby Tregs enter the skin remain poorly understood. The aim of this study was to use intravital microscopy to investigate adhesion and transmigration of Tregs in the dermal microvasculature in a two-challenge model of contact sensitivity. Using intravital confocal microscopy of Foxp3-GFP mice, we visualized endogenous Tregs and assessed their interactions in the dermal microvasculature. Four ...
Leukocyte migration is the hallmark of inflammation in vivo, and αMβ2 and Fg have been shown to contribute to leukocyte migration in multiple systems (23)(24). This study has used αMβ2 transfectants and selected mutants to dissect the molecular requirements for αMβ2-mediated cell migration to Fg and its derivatives. The major conclusions of our study are the following. (a) Fg supports a chemotactic cell migration mediated by αMβ2. This response is dependent on Fg concentration and occurs at low (1-50 μg/ml) Fg levels. (b) The αM I domain is necessary but not sufficient to support cell migration to Fg. In contrast to cell adhesion to Fg, efficient migration requires the β2 subunit. (c) The P1 and P2 peptides, as well as the D100 fragment, support cell migration. Thus, the same Fg derivatives that mediate αMβ2-dependent cell adhesion also support cell migration. (d) The P2 peptide stimulates αMβ2-mediated cell migration to Fg and the P1 peptide, in a manner similar to other αMβ2 ...
Would you like to study Behaviour & Social Culture or Business and Economics? All information about Introduction to Migration Studies in Maastricht: admission requirements, deadlines and grants.
Directed cell migration is usually thought to depend on the presence of long-range gradients of either chemoattractants or physical properties such as stiffness or adhesion. However, in vivo, chemical or mechanical gradients have not systematically been observed. Here we review recent in vitro exper …
We have previously shown that BMP4 reduces proliferation and increases migration of breast cancer cells in vitro [10]. As these results were derived from cells grown in 2D monolayer culture, we set out to analyze the effect of BMP4 in a more physiological setting by employing 3D culture systems. We approached this issue by using both a biological gel (Matrigel, the standard 3D culture environment) and a synthetic material with RGD peptides and MMP-degradable peptide links (PEG gel).. The two materials studied provided dissimilar 3D environments as first evidenced by differences in the morphology of the normal and cancer cell clusters. The MCF-10A normal mammary epithelial cells had a polarized acini structure in Matrigel, as previously shown [17], while in PEG gel the cells formed irregular non-polarized structures. Similarly, the morphology of the different cancer cells varied between the two 3D models, with the structures formed in Matrigel again corresponding to those previously reported ...
Effect of TGFβ1 on the phenotype, migratory ability, and survival of CD16− monocytes. PBMCs were depleted of CD16+ cells using miniMACS magnetic selection. T
Course IA (p85/p110) phosphoinositide three-kinases play A serious function in regulating cell advancement, survival, and motility. Activating mutations during the p110alpha isoform of the class IA catalytic subunit (PIK3CA) are generally found in human cancers. These mutations lead to elevated proliferation and transformation in cultured cells, but their effects on cell motility and tumor metastasis have not been evaluated. We utilized lentiviral-mediated gene transfer and knockdown to create secure MDA-MB-231 cells wherein the endogenous human p110alpha is replaced with both wild-variety bovine p110alpha or the two most frequent activating p110alpha mutants, the helical area mutant E545K along with the kinase area mutant H1047R. The phosphoinositide 3-kinase/Akt pathway was hyperactivated in cells expressing physiologic levels of helical or kinase domain mutants ...
TY - JOUR. T1 - Group choreography. T2 - Mechanisms orchestrating the collective movement of border cells. AU - Montell, Denise J.. AU - Yoon, Wan Hee. AU - Starz-Gaiano, Michelle. PY - 2012/10/1. Y1 - 2012/10/1. N2 - Cell movements are essential for animal development and homeostasis but also contribute to disease. Moving cells typically extend protrusions towards a chemoattractant, adhere to the substrate, contract and detach at the rear. It is less clear how cells that migrate in interconnected groups in vivo coordinate their behaviour and navigate through natural environments. The border cells of the Drosophila melanogaster ovary have emerged as an excellent model for the study of collective cell movement, aided by innovative genetic, live imaging, and photomanipulation techniques. Here we provide an overview of the molecular choreography of border cells and its more general implications.. AB - Cell movements are essential for animal development and homeostasis but also contribute to ...
Background: Cell invasion through extracellular matrix (ECM) is a critical step in tumor metastasis. To study cell invasion in vitro, the internal microenvironment can be simulated via the application of 3D models. Results: This study presents a method for 3D invasion examination using microcarrier-based spheroids. Cell invasiveness can be evaluated by quantifying cell dispersion in matrices or tracking cell movement through time-lapse imaging. It allows measuring of cell invasion and monitoring of dynamic cell behavior in three dimensions. Here we show different invasive capacities of several cell types using this method. The content and concentration of matrices can influence cell invasion, which should be optimized before large scale experiments. We also introduce further analysis methods of this 3D invasion assay, including manual measurements and homemade semi-automatic quantification. Finally, our results indicate that the position of spheroids in a matrix has a strong impact on cell ...
All-and genes, ATRA activates a RAR-dependent epithelial differentiation program. pro-migratory determinant to an anti-migratory mediator. Inhibition of the Level1 path not really just takes on a part in the anti-migratory actions of ATRA; it is usually relevant also for the … Continue reading →. ...
Vol 10: Propagating Waves of Directionality and Coordination Orchestrate Collective Cell Migration.. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
AbstractMalignant pleural mesothelioma (MPM) is a devastating malignancy characterized by invasive growth and rapid recurrence. The identification and inhibition of molecular components leading to this migratory and invasive phenotype are thus essential. Accordingly, a genome-wide expression array a
Examples of collective cell migration. First column: schematic representation of different migratory types. The regions where cells are interacting are depicted
miR-21 is a key molecule in a wide range of cancers, and identifying its functional role in BC has direct clinical implications. We show here that knockdown of miR-21 suppresses cell growth and proliferation of MCF-7 cells in vitro, and suppresses MCF-7 xenograft growth. This result is consistent with the findings of Si et al. [9]. Interestingly, our study suggests that LNA-antimiR-21 also suppresses the growth and proliferation of MDA-MB-231 in vitro, in contrast to a recent report that found no effect of LNA-antimiR-21 on the growth of MDA-MB-231 in vitro or in vivo, although anti-miR-21-treated tumors were slightly smaller than control tumors [10]. One possibility could be differences in transfection efficiency, or miRNA ASO potency. Our results suggest that, as an oncomir, miR-21 also affects cell migration.. MCF-7 cells are hormone-sensitive and difficult to culture in vivo. Therefore, we used 17-estradiol to facilitate MCF-7 cells growth in nude mice, which is a common technique. Recently, ...
Cell migration is a basic developmental function that serves to build tissues, organs, and whole animals. Defects in cell migration are associated with birth defects and cancer, in particular the metastasis of tumors. Over the past forty years researchers have used the fruit fly to understand the genetic basis of development, including cell migration, but many of the tools and approaches used are beyond the skills and understanding of an undergraduate and advanced high school lab. We have developed a practical lab that allows students to use fly oogenesis to understand how genes regulate cell migration. Students learn to sort males from females, recognize fly genetic markers to identify wild type and mutant animals, hand-dissect ovaries, perform histochemical staining to reveal gene expression in this tissue, and visualize normal and aberrant cell migration using light microscopy to distinguish the effect of a key mutation in a gene required for cell migration. From this approach, students learn ...
TY - JOUR. T1 - Comparative analysis of the role of small G proteins in cell migration and cell death. T2 - Cytoprotective and promigratory effects of RalA. AU - Jeon, Hyejin. AU - Zheng, Long Tai. AU - Lee, Shinrye. AU - Lee, Won Ha. AU - Park, Nammi. AU - Park, Jae-Yong. AU - Heo, Won Do. AU - Lee, Myung Shik. AU - Suk, Kyoungho. PY - 2011/1/1. Y1 - 2011/1/1. N2 - Small G protein superfamily consists of more than 150 members, and is classified into six families: the Ras, Rho, Rab, Arf, Ran, and RGK families. They regulate a wide variety of cell functions such as cell proliferation/differentiation, cytoskeletal reorganization, vesicle trafficking, nucleocytoplasmic transport and microtubule organization. The small G proteins have also been shown to regulate cell death/survival and cell shape. In this study, we compared the role of representative members of the six families of small G proteins in cell migration and cell death/survival, two cellular phenotypes that are associated with ...
Tumor cell migration is a key step in the formation of cancer metastasis. The mammalian target of rapamycin (mTOR), a highly conserved and ubiquitously expressed serinethreonine kinase, has been intensely studied for over a decade as a central regulator of cell growth, proliferation, differentiation, and survival. Recent data have shown that mTOR also plays a critical role in the regulation of tumor cell motility and cancer metastasis. Here, we briefly review recent advances regarding mTOR signaling in tumor cell motility. We also discuss recent findings about the mechanism by which rapamycin, a specific inhibitor of mTOR, inhibits cell motility in vitro and metastasis in vivo.. ...
Gersende Alphonse is the author of these articles in the Journal of Visualized Experiments: Isolation and Characterization of a Head and Neck Squamous Cell Carcinoma Subpopulation Having Stem Cell Characteristics, Evaluation of the Cell Invasion and Migration Process: A Comparison of the Video Microscope-based Scratch Wound Assay and the Boyden Chamber Assay
Cell movement has essential functions in development, immunity and cancer. Various cell migration patterns have been reported, such as Brownian motion, intermittent and persistent random-walks, but no general rule has emerged so far. Here, we show on the basis of experimental data in vitro and in vivo that cell persistence, which quantifies the straightness of trajectories, is robustly coupled to cell migration speed. We suggest that this universal coupling constitutes a generic law of cell migration, which originates in the advection of polarity cues by an actin cytoskeleton undergoing flows at the cellular scale. Our analysis relies on a theoretical model that we validate by measuring the persistence of cells upon modulation of actin flow speeds. Beyond the quantitative prediction of the coupling, the model yields a generic phase diagram of cellular trajectories, which recapitulates the full range of observed migration patterns. Recent extensions of this model describe the oscillatory motion ...
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If you have a question about this talk, please contact Emma Copley.. Host: Dr Bidesh Mahata ([email protected]). Abstract not available. This talk is part of the Immunology in Pathology series.. ...
TY - JOUR. T1 - Involvement of cysteine-rich protein 61 in the epidermal growth factor-induced migration of human anaplastic thyroid cancer cells. AU - Chin, Li Han. AU - Hsu, Sung Po. AU - Zhong, Wen-Bin. AU - Liang, Yu Chih. PY - 2016. Y1 - 2016. N2 - Anaplastic thyroid cancer (ATC) is among the most aggressive types of malignant cancer. Epidermal growth factor (EGF) plays a crucial role in the pathogenesis of ATC, and patients with thyroid carcinoma typically exhibit increased cysteine-rich protein 61 (Cyr61). In this study, we found that EGF treatment induced cell migration, stress fiber formation, Cyr61 mRNA and protein expressions, and Cyr61 protein secretion in ATC cells. The recombinant Cyr61 protein significantly induced cell migration; however, inhibition of Cyr61 activity by a Cyr61-specific antibody abrogated EGF-induced cell migration. EGF treatment also affected epithelial-to-mesenchymal transition (EMT)-related marker protein expression, as evidenced by an increase in vimentin and ...
T-LIF - T Lymphocyte Migration Inhibitory Factors. Looking for abbreviations of T-LIF? It is T Lymphocyte Migration Inhibitory Factors. T Lymphocyte Migration Inhibitory Factors listed as T-LIF
Our previous studies have demonstrated that epidermal growth factor (EGF) can induce cell migration through the induction of cysteine-rich protein 61 (Cyr61) in human anaplastic thyroid cancer (ATC) cells. The aim of the present study was to determine the inhibitory effects of combined treatment with the peroxisome proliferator-activated receptor-γ (PPARγ) ligand troglitazone and the cholesterol-lowering drug lovastatin at clinically achievable concentrations on ATC cell migration. Combined treatment with 5 μM troglitazone and 1 μM lovastatin exhibited no cytotoxicity but significantly inhibited EGF-induced migration, as determined using wound healing and Boyden chamber assays. Cotreatment with troglitazone and lovastatin altered the epithelial-to-mesenchymal-transition (EMT) -related marker gene expression of the cells; specifically, E-cadherin expression increased and vimentin expression decreased. In addition, cotreatment reduced the number of filopodia, which are believed to be involved in
Alterations in cell migration are a hallmark of cancer cell invasion and metastasis. In vitro assays commonly used to study cell migration, including the scratch wound healing assay, Boyden chamber assay, and newly developed advanced systems with microfluidics, each have several disadvantages. Here we describe an easy and cost-effective in vitro assay for cell migration employing cloning rings to create gaps in the cell monolayer (
TY - JOUR. T1 - Rho GTPase. T2 - A molecular compass for directional cell migration. AU - Senoo, Hiroshi. AU - Iijima, Miho. N1 - Funding Information: We are grateful to H Sesaki for critically reading the manuscript. This work was supported by a NIH grant (GM084015). Copyright: Copyright 2014 Elsevier B.V., All rights reserved.. PY - 2013. Y1 - 2013. N2 - Ras GTPases and phosphatidylinositol 3-kinases mediate intracellular signaling in directed cell migration. During chemotaxis, cells spatially control the activation of Ras/ PI (3,4,5)-trisphosphate (PIP3) signaling and translate extracellular chemical gradients into intracellular signal cascades. This process is called directional sensing, and enables persistent cell migration with extraordinary sensitivity in shallow, unstable gradients of chemoattractants. In our recent study, we identified a Rho GTPase and its guanine nucleotide exchange factor (GEF) as molecular modulators that transmit signals from G protein-coupled receptors to Ras/PIP3 ...
Background: Tumor spreading is the major threat for cancer patients. The recently published anti-cancer drug salinomycin raised hope for an improved treatment by targeting therapy-refractory cancer stem cells. However, an unambiguous role of salinomycin against cancer cell migration and metastasis formation remains elusive. Findings: We report that salinomycin effectively inhibits cancer cell migration in a variety of cancer types as determined by Boyden chamber assays. Additionally, cells were treated with doxorubicin at a concentration causing a comparable low cytotoxicity, emphasizing the anti-migratory potential of salinomycin. Moreover, single-cell tracking by time-lapse microscopy demonstrated a remarkable effect of salinomycin on breast cancer cell motility. Ultimately, salinomycin treatment significantly reduced the metastatic tumor burden in a syngenic mouse tumor model. Conclusions: Our findings clearly show that salinomycin can strongly inhibit cancer cell migration independent of the ...
The secreted semaphorin Sema3E controls cell migration and invasiveness in cancer cells. conversely RNAi-based knock-down or pharmacological inhibition of Notch signaling by gamma-secretase inhibitors mogroside IIIe downregulated PlexinD1 amounts. Notably both Notch1 and Notch3 appearance favorably correlates with PlexinD1 amounts in prostate cancers as well such as additional tumor types. In prostate malignancy cells Sema3E-PlexinD1 axis was previously reported to regulate migration; however implicated mechanisms were not elucidated. Here we display that in these cells PlexinD1 activity induces the manifestation of the transcription element Slug downregulates E-cadherin levels and enhances cell migration. Moreover our mechanistic data determine PlexinD1 mogroside IIIe like a pivotal mediator of this signaling axis downstream of Notch in prostate malignancy cells. In fact on one hand PlexinD1 is required to mediate cell migration and E-cadherin rules elicited by Notch. On the other hand PlexinD1 ...
Hypoxia is known to regulate the expression of genes involved in the migration of various cell types. Although many studies have shown that hypoxia increases cell migration, it still remains unclear whether hypoxia could modulate the stromal cell derived factor-1 (SDF-1)-dependent migration of leukemic cell. Herein, we demonstrated that the SDF-1-dependent migration of HL-60, was reduced under hypoxia with no comparable decrease of CXC-type chemokine receptor CXCR4, a cognate receptor for SDF-1. Furthermore, we showed that migration toward SDF-1 was reduced by inactivation of either serine/threonine kinase Akt or extracellular signal regulated kinase Erk, which was confirmed by selective pathway inhibitor LY294002 and PD98059. In our results, phosphorylation of Erk was increased under hypoxia, but phosphorylation of Akt was attenuated on the contrary. These results led us to conclusion that hypoxia could inhibit the SDF-1-dependent migration of HL-60 via blocking of Akt activation ...
Collective cell movement depends on intracellular biological mechanisms as well as environmental cues due to the extracellular matrix (1⇓⇓⇓-5), mainly composed of collagen which is organized in hierarchical structures, such as fibrils and fibers. The mechanical properties of collagen fibril networks are essential to offer little resistance and high sensitivity to small deformations, allowing easy local remodeling and strong strain stiffening needed to ensure cell and tissue integrity (6). Wound healing is a typical biological assay to study collective migration of cells under controlled conditions in vitro and is a prototypical experimental method to study active matter (7⇓⇓-10). Experiments performed on soluble collagen (11) or other gels (12), micropatterned (13, 14) and deformable substrates (1) show that cell migration is guided by the substrate structure and stiffness (5, 15, 16).. It has been argued that collective migration properties arise from stresses transmitted between ...
Neural crest cells are both highly migratory and significant to vertebrate organogenesis. However, the signals that regulate neural crest cell migration remain unclear. In this study, we test the function of differential screening-selected gene aberrant in neuroblastoma (DAN), a bone morphogenetic protein (BMP) antagonist we detected by analysis of the chick cranial mesoderm. Our analysis shows that, before neural crest cell exit from the hindbrain, DAN is expressed in the mesoderm, and then it becomes absent along cell migratory pathways. Cranial neural crest and metastatic melanoma cells avoid DAN protein stripes in vitro. Addition of DAN reduces the speed of migrating cells in vivo and in vitro, respectively. In vivo loss of function of DAN results in enhanced neural crest cell migration by increasing speed and directionality. Computer model simulations support the hypothesis that DAN restrains cell migration by regulating cell speed. Collectively, our results identify DAN as a novel factor ...
Morphogenetic movements such as cell migration are crucial for the development of multicellular organisms. Cells that are born at distinct locations in the developing animal often undergo precise, spatiotemporally regulated migration to distant sites where they eventually build specialized tissues and organs. How input from multiple signaling pathways is coordinated to ensure proper cell movement remains one of the main challenges in the field of cell migration and developmental biology.. The migration of border cells (BCs) in the Drosophila egg chamber provides a unique system with which to genetically dissect the mechanisms regulating invasive cell migration in vivo (Montell, 2003; Rorth, 2002). During oogenesis, a group of approximately eight cells, called BCs, is specified at the anterior pole of the ovarian follicular epithelium (Montell et al., 1992). At stage 9 of oogenesis, BCs change their shape, exit the epithelium and become migratory (Fig. 1A). BCs comprise two inner cells, called ...
TDE0214-mediated regulation of motility.PilZ domain proteins have been studied in several motile bacteria, and they are often implicated in regulation of cell motility (12, 13, 26-28). In these bacteria, mutations in the genes encoding those c-di-GMP effectors have different effects on cell motility. For instance, disruptions of B. burgdorferi plzA and V. cholerae plzB impair the cell motility (27, 28). In contrast, mutations of E. coli ycgR and Caulobacter crescentus dgrA or dgrB have no impact on the wild-type cell motility (12, 13, 70). Instead, mutations in these three genes can relieve the inhibition of motility that is caused by either deletions of PDE proteins or overexpression of DGC proteins, highlighting that these PilZ domain proteins affect cell motility only at conditions where the level of c-di-GMP is elevated (12, 13, 26). In this report, we found that inactivation of TDE0214 impaired the cell motility (Fig. 4; see also Movies S1 and S2 in the supplemental material), which is ...
Quantifying the ability of a compound to modulate cell migration rate is a crucial part of many studies including those on chemotaxis, wound healing and cancer metastasis. Existing migration assays all have their strengths and weaknesses. The scratch assay is the most widely used because it seems appealingly simple and inexpensive. However, the scratch assay has some important limitations, as the tool introducing the wound might injure/stress the boundary cells and/or harm underlying matrix coatings, which in both cases will affect cell migration. This described method is a Cell Exclusion Zone Assay, in which cell-free areas are created by growing cells around removable silicone stoppers. Upon appropriate staining with fluorescent dyes and microscopically visualizing the monolayers, the migration rate is then quantified by counting the cells (nuclei) intruding the void area left by the silicone insert. In the current study human small intestine epithelial cells were seeded on a physiological ...
Many human cancers express elevated levels of cyclooxygenase-2 (COX-2), an enzyme responsible for the biosynthesis of prostaglandins. Available clinical data establish the protective effect of COX-2 inhibition on human cancer progression. According to the study by Medical College of Georgia, showed that the COX-2 product prostaglandin E(2) (PGE(2)) acts on cognate receptor EP4 to promote the migration of A549 lung cancer cells. Treatment with PGE(2) enhances tyrosine kinase c-Src activation, and blockade of c-Src activity represses the PGE(2)-mediated lung cancer cell migration. PGE(2) affects target cells by activating four receptors named EP1 to EP4. Use of EP subtype-selective ligand agonists suggested that EP4 mediates prostaglandin-induced A549 lung cancer cellmigration, and this conclusion was confirmed using a short hairpin RNA approach to specifically knock down EP4 expression(7 ...
Collective cell migration is involved in development, wound healing and metastasis. In the Drosophila ovary, border cells (BC) form a small cluster that migrates collectively through the egg chamber. To achieve directed motility, the BC cluster coordinates the formation of protrusions in its leader cell and contractility at the rear. Restricting protrusions to leader cells requires the actin and plasma membrane linker Moesin. Herein, we show that the Ste20-like kinase Misshapen phosphorylates Moesin in vitro and in BC. Depletion of Misshapen disrupts protrusion restriction, thereby allowing other cells within the cluster to protrude. In addition, we show that Misshapen is critical to generate contractile forces both at the rear of the cluster and at the base of protrusions. Together, our results indicate that Misshapen is a key regulator of BC migration as it coordinates two independent pathways that restrict protrusion formation to the leader cells and induces contractile forces.. ...
MDGA proteins have been studied in humans (De Juan et al., 2002; Díaz-López et al., 2005), rats (Litwack et al., 2004), mice (Takeuchi et al., 2007), chickens (Fujimura et al., 2006) and medaka (Sano et al., 2009). Here we identified and cloned three MDGA orthologs in zebrafish, MDGA1, MDGA2A and MDGA2B. We found MDGA2A to be expressed in a subset of motoneurons, especially in the ones of the cranial, trigeminal and facial nerves. Morpholino mediated knockdown of MDGA2A led to aberrant cell migration of trigeminal neurons and to defasciculation and increased branch formation of the trigeminal as well as facial nerve. These results demonstrate that MDGA2A interactions are necessary for proper migration, axon outgrowth and bundling in cranial motoneurons.. In agreement with our current findings, MDGAs in other species have already been implicated in neuronal migration and axon guidance. In rats, MDGA positive cells were found in the pontine migratory stream, suggesting that these ...
Supplementary Materials Supplemental Materials supp_28_14_1924__index. highly associated with enhanced speed and persistence Bmp6 of directional movement. Strikingly, WRAMP structures form transiently, with cells displaying directional persistence during periods when they are present and cells changing directions randomly when they are absent. Cells appear to pause locomotion when WRAMP structures disassemble and then migrate in new directions after reassembly at a different location, which forms the new rear. We conclude that WRAMP structures represent a rear-directed cellular mechanism to control directional migration and that their ability to form dynamically within cells may ML-323 control changes in direction during extended migration. INTRODUCTION ML-323 Cell movement requires the spatial control of signal transduction, including cell polarity mechanisms that move proteins to specific intracellular locations (Huttenlocher, 2005 ; McCaffrey and Macara, 2012 ). During cell locomotion, cells ...
Fingerprint Dive into the research topics of Evaluation of pancreatic cancer cell migration with multiple parameters in vitro by using an optical real-time cell mobility assay device. Together they form a unique fingerprint. ...
Dive into the research topics of Glycidamide promotes the growth and migratory ability of prostate cancer cells by changing the protein expression of cell cycle regulators and epithelial-to-mesenchymal transition (EMT)- associated proteins with prognostic relevance. Together they form a unique fingerprint. ...
To study the physiological role of L-selectin shedding in lymphocyte biology, we have mutagenized the cleavage site of mouse L-selectin and directed the expression of mutant or WT L-selectin to T lymphocytes by transgenesis. L-Selectin transgenic mice were bred with L-selectin KO mice to generate lines in which either WT or nonshedding L-selectin was only expressed on T lymphocytes, and lines expressing physiological levels of L-selectin at the cell surface were selected for lymphocyte migration studies. We deleted the Ly22 epitope recognized by mAb T28 to distinguish transgenic from endogenous L-selectin during backcrossing to L-selectin KO mice. The anti-Ly22 antibody T28 inhibits L-selectin-dependent binding to PLNs in the frozen section assay (31). However, we could detect no differences in the function of transgenic Ly22− (WT) and endogenous Ly22+ (C57BL/6) L-selectin either in rolling assays or in short-term trafficking to PLNs. We have compared the migration pathways of T cells ...
The migration of multiple cells as a cooperativeunit known as collective cell migration is a common phenomenon in development, cancer and healing
Skin cell migration is essential for skin wound healing. Steps for cell migration are often disrupted in non‐healing wounds, causing patient morbidity and even fatality. Currently‐available treatments are unsatisfactory. To identify novel wound‐healing targets, we took two approaches. First, we studied the migratory gene profiles in human keratinocytes (HKs). Second, we investigated secreted molecules from TGFalpha‐stimulated human keratinoytes, which contained a strong motogenic, but not mitogenic, activity. In the first study, the main challenge is to separate genes that are often simultaneously induced by pleiotropic signals of a given growth factor, including migration, proliferation and metabolism. Therefore, we designed the following steps. First, we took advantage of a unique response of HKs to TGF‐beta, which inhibits proliferation but not migration of the cells, to suppress selectively the proliferation signal‐responding genes. Second, we independently stimulated HKs with ...
Although an increased expression level of XIAP is associated with cancer cell metastasis, the underlying molecular mechanisms remain largely unexplored. To verify the specific structural basis of XIAP for regulation of cancer cell migration, we introduced different XIAP domains into XIAP−/− HCT116 cells, and found that reconstitutive expression of full length HA-XIAP and HA-XIAP ΔBIR, both of which have intact RING domain, restored β-Actin expression, actin polymerization and cancer cell motility. Whereas introduction of HA-XIAP ΔRING or H467A mutant, which abolished its E3 ligase function, did not show obvious restoration, demonstrating that E3 ligase activity of XIAP RING domain played a crucial role of XIAP in regulation of cancer cell motility. Moreover, RING domain rather than BIR domain was required for interaction with RhoGDI independent on its E3 ligase activity. To sum up, our present studies found that role of XIAP in regulating cellular motility was uncoupled from its caspase
TY - JOUR. T1 - NHE3 phosphorylation via PKCη marks the polarity and orientation of directionally migrating cells. AU - Ozkucur, Nurdan. AU - Song, Bing. AU - Bola, Sharanya. AU - Zhang, Lei. AU - Reid, Brian. AU - Fu, Guo. AU - Funk, Richard H W. AU - Zhao, Min. PY - 2014/12/1. Y1 - 2014/12/1. N2 - Endogenous electric fields (EF) may provide an overriding cue for directional cell migration during wound closure. Perceiving a constant direction requires active sodium-hydrogen exchanger (pNHE3) at the leading edge of HEK 293 cells but its activation mechanism is not yet fully understood. Because protein kinase C (PKC) is required in electrotaxis, we asked whether NHE3 is activated by PKC during wound healing. Using pharmacological (pseudosubstrate and edelfosine) inhibition, we showed that inhibition of PKCη isoform impairs directional cell migration in HEK 293 cells in the presence of a persistent directional cue (0.25-0.3 V/mm of EF for 2 h). Further, we found that pNHE3 forms complexes with ...
Product Manual Radius 24-Well Cell Migration Assay (Laminin Coated) Catalog Number CBA-125-LN 24 assays FOR RESEARCH USE ONLY Not for use in diagnostic procedures Introduction Cell migration is a highly
MDM2 is an E3 ubiquitin ligase that binds and ubiquitinates the tumor suppressor protein p53, leading to its proteasomal degradation. Nutlin-3a (Nutlin) is a preclinical drug that binds MDM2 and prevents the interaction between MDM2 and p53, leading to p53 stabilization and activation of p53 signaling events. Previous studies have reported that Nutlin promotes growth arrest and/or apoptosis in cancer cells that express wild-type p53. In the current study, Nutlin treatment caused a cytoskeletal rearrangement in p53 wild-type human cancer cells from multiple etiologies. Specifically, Nutlin decreased actin stress fibers and reduced the size and number of focal adhesions in treated cells. This process was dependent on p53 expression but was independent of p21 expression and growth arrest. Consistent with this, Nutlin-treated cells failed to form filamentous actin-based motility structures (lamellipodia) and displayed significantly decreased directional persistence in response to migratory cues. ...
eicosapentaenoic acid as fish oil) effects the level of burnout from the n-3 fatty acids can decrease NK cell (natural killer cell) activity in healthy subjects, a modulator of the less inflamitory that has little or no effect on cell motility. Including large blocks of micro- and minisatellites Alu-repeats closing the gaps in chromosome 19, (during the final stage of the Human Genome Project) YAC yeast artificial chromosome, is for activating the cytotoxicity of natural killers NK. The inflammatory (20:3 ω-6) the presence in steps (dietary oils 18:2n-6, 18:3n-6,20:3n-6, 18:2n-6,20:5n-3 and 22:5n-3and 20:5n-3, 20:4n-6 and 20:5n-3 showed a histopathological lesion indicative of lipoid liver degeneration till…) of a food supply move forward for a certain distance a random walk and the amount needed to code for amino acids is taking a step in the right direction also known as social gliding motility or a worse random walk sensing. Via isolated normal sweat ducts, epithelial sodium channel (ENaC; ...
Durotaxis is a form of cell migration in which cells are guided by rigidity gradients, which arise from differential structural properties of the extracellular matrix (ECM). Most normal cells migrate up rigidity gradients (in the direction of greater stiffness). The process of durotaxis requires a cell to actively sense the environment, process the mechanical stimulus, and execute a response. Originally, this was believed to be an emergent metazoan property, as the phenomenon requires a complex sensory loop that is dependent on the communication of many different cells. However, as the wealth of relevant scientific literature grew in the late 1980s and throughout the 1990s, it became apparent that single cells possess the ability to do the same. The first observations of durotaxis in isolated cells were that mechanical stimuli could cause the initiation and elongation of axons in the sensory and brain neurons of chicks and induce motility in previously stationary fish epidermal keratocytes. ECM ...
A new study published in Nature Communications could help biologists understand how various types of migratory cells, such as immune cells, find their way through tissues in the human body. The research, by scientists at McGill University in Montreal and the Radboud University Medical Center in the Netherlands, focuses on a complex of proteins, known as podosomes, found in the membrane of migratory cells and in certain invasive cancer cells. In essence, podosomes mechanically push on the cell membrane, enabling the cell to probe its surroundings and select its migration path through the tissue matrix. Previous studies of cells in tissue culture have shown that individual podosomes occur in a network or cluster where their components assemble and disassemble rapidly in migrating cells. Visually, the networks look like city hubs (podosomes) connected by road-like spokes, composed of actin cytoskeleton filaments. Biologists have been trying to understand the complex dynamics and function of these networks
During activation in response to injury and inflammation, microglial cells can actively migrate into the damaged region of the brain. To fulfill this function, microglia bear receptors for motility factors such as IL-10, epidermal growth factor, complement 5A, and hyaluronan (Turley et al., 1994; Nolte et al., 1996, 1997; Huettner et al., 1997). C13NJ microglial cells represent an interesting model to study cell migration because wound healing is rapidly achieved when chemoattractant factors that are present in 10% serum are added. However, to avoid the possible contribution of cell proliferation to the migration, we performed the assay in the absence of serum. Under these conditions, NT (10 nm) induces a marked activation of cell migration with an effect representing ∼35% of that measured in the presence of serum. An identical result was obtained by using the modified Boyden chamber. Although the NT effect on cell migration defined using the chemotaxis assay was totally blocked by both PI ...
The standard Oris™ assay protocol was followed with 30,000 ECFC cells per well. These slow-adhering cells were allowed to attach overnight, then stoppers were removed and culture medium containing Dasatinib to the indicated concentrations was added. Cells were incubated for 24 hours and migration was quantified by measuring the percent area closure. Percent inhibition was then calculated as [(area of cell migration in controls - area of migration in drug treated cells) / (area of cell migration in controls - area of cell migration in samples treated with maximum concentration of drug)]. Standard deviations are for averages of four data points per drug concentration for Oris™ and eight per drug for scratch. Z-factors were 0.7 for Oris™ vs 0.2 for scratch assays (see reference).. Oris™ assays generate more robust data to:. ...
Cell migration or movement is a highly dynamic cellular process, requiring precise regulation that is essential for a variety of biological processes. microRNAs (miRNAs) are a class of tiny non-coding RNA molecules that function as critical post-transcriptional regulators of gene expression. Emerging evidence demonstrates that miRNAs play important roles in cell migration and directly contribute to extracellular matrix (ECM) remodeling, cell adhesion, and cell signalling that controls cell migration by targeting a large number of protein-coding genes. Accordingly, the dysregulation of these miRNAs has been linked to several migration-related diseases. In this review, we summarize and highlight the recent advances concerning the roles and validated targets of miRNAs in the control of cell movement.
The purpose of this study was to investigate invasion and metastasis related genes in gastric cancer. The transwell migration assay was used to select a highly invasive sub-line from minimally invasive parent gastric cancer cells, and gene expression was compared using a microarray. MMP28 upregulation was confirmed using qRT-PCR. MMP28 immunohistochemistry was performed in normal and gastric cancer specimens. Invasiveness and tumor formation of stable cells overexpressing MMP28 were tested in vitro and in vivo. MMP28 was overexpressed in the highly invasive sub-cell line. Immunohistochemistry revealed MMP28 expression was markedly increased in gastric carcinoma relative to normal epithelia, and was significantly associated with depth of tumor invasion, lymph node metastasis and poorer overall survival. Ectopic expression of MMP28 indicated MMP28 promoted tumor cell invasion in vitro and increased gastric carcinoma metastasis in vivo. This study indicates MMP28 is frequently overexpressed during
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Actin-based cell migration is a key process for morphogenesis, wound healing and cancer invasion [1]. Cell migration has been extensively studied on two-dimensional (2D) substrates. It typically involves a combination of front protrusion, rear contraction and graded adhesion [1]. At the leading edge, actin polymerization forms flat and wide protruding lamellipodia [2]. At the rear, myosin-induced contraction and disassembly of the actin networks generate contraction and forward translocation of the cell body [2]. Dynamic adhesions [3,4] are formed in the lamellipodia region, mature and disassemble as they move towards the centre of the cell [5]. The migration speed of cells is determined by a delicate balance among actin polymerization, myosin-powered retrograde actin flow, and an effective adhesion drag [6].. In a more physiologically relevant three-dimensional (3D) environment, however, cell migration is far less understood due to both the technical challenges and the complexity of migratory ...
The ordered, directional migration of T-lymphocytes is a key process during immune surveillance, and immune response. T-cell migration is a complex, highly coordinated process. This requires cell adhesion to the high endothelial venules or to the extracellular matrix by a series of surface receptor/ligand interactions involving adhesion molecules of the integrin family including lymphocyte function associated molecule-1 (LFA-1), phosphorylation- dependent signalling cascades and cytoskeletal rearrangements. Mechanisms that regulate T-cell migration are of considerable relevance for understanding the pathogenesis of various diseases including chronic inflammatory diseases such as inflammatory bowel disease and the inflammatory arthropathies ...
Time lapse confocal imaging has been an essential method to investigate the 3D dynamic behaviors of cells in tissue cultures. For long-term live cell imaging, it is critical to reduce phototoxic damage to the cells caused by repeated laser scanning. Yokogawa CSU (confocal scanner unit) is a confocal unit using a microlens-enhanced dual Nipkow disk confocal optical system, which has been shown to be less harmful to living cells compared to conventional single beam scanning devices. The CQ1 is an all-in-one confocal quantitative imaging cytometer based on the CSU. Here we report the 3D time lapse live cell imaging in a multilayered cell sheet using CQ1.
Time lapse confocal imaging has been an essential method to investigate the 3D dynamic behaviors of cells in tissue cultures. For long-term live cell imaging, it is critical to reduce phototoxic damage to the cells caused by repeated laser scanning. Yokogawa CSU (confocal scanner unit) is a confocal unit using a microlens-enhanced dual Nipkow disk confocal optical system, which has been shown to be less harmful to living cells compared to conventional single beam scanning devices. The CQ1 is an all-in-one confocal quantitative imaging cytometer based on the CSU. Here we report the 3D time lapse live cell imaging in a multilayered cell sheet using CQ1.
Figure 6. Dynamic effects of LINC01140 and miR-140-5p on bladder cancer cell aggressiveness and macrophage M2 polarization T24 cells were cotransfected with si-LINC01140 and anti-miR-140-5p and examined for (A) the cell viability by MTT assay; (B) protein levels of FGF9, ki-67, MMP-2, and MMP-9 by immunoblotting; (C) migration capacity by wound healing assay; and (D) invasive capacity by Transwell assay. (E, F) T24 cells were cotransfected with si-LINC01140 and anti-miR-140-5p and the culture medium (shown in the figures as conditioned medium (CM) si-NC + anti-NC, si-LINC01140 + anti-NC, si-NC + anti-miR-140-5p, and si-LINC01140 + anti-miR-140-5p) was collected for macrophage incubation. M0 macrophages were cultured in the above-described four kinds of CMs and polarized to M1 or M2, respectively, and examined for (E) the protein levels of CD206 and CD16 by immunoblotting. (F) The concentrations of IL-10, Arg1, iNOS, and TNF-α in the macrophage culture medium was determined by ELISA. *P,0.05, ...
It has been reported that HAX1 is a multi-functional protein which protects cells from apoptosis, modulates autophagy, regulates membrane protein trafficking and promotes cell migration. Many studies have shown it has many different intra-cellular binding partners (including integrin β6 subunit) and exists in multiple cellular locations, including the nucleus, mitochondria and cytoplasm. This behaviour seemed unlikely for a single protein. My lab discovered that there are at least eight different HAX1 isoforms in humans and this might explain why multiple roles and sub-cellular locations are described for HAX1. In this study, I sought not only to confirm the role of HAX1 in cell behaviour, but also to examine specifically the role of HAX1 isoforms in different biological functions. I screened a panel of cancer cell lines for αvβ6-dependent migration, including breast (MCF10.CA1a), pancreatic (CFPac1 and Panc04.03), and αvβ1-dependent migration in cervical cancer (HeLa); siRNA designed to ...
Our central finding is that a relatively small change in total Rac1 activity can serve as a switch that regulates the overall intrinsic pattern of cell migration of a cell. By using at least three different approaches (mutagenesis, RNA interference, and manipulation of the extracellular environment between 2D and 3D), we demonstrate that moderate levels of active Rac support random motility by selectively promoting peripheral lamellae that permit cell turning, but reductions of active Rac by ≥30% instead support directionally persistent migration using axial lamellae.. This role of Rac in regulating the capacity for random versus directionally persistent motility was found for a variety of cell types, including fibroblasts and epithelial cells, suggesting that it is a common phenomenon. Moderate changes in Rac activity did not necessarily affect the velocity of cell migration, and in a 3D environment, suppression of Rac activity occurred together with increased velocity, indicating the ...
Cell motility is essential for many morphogenetic and regenerative processes, also contributing to the development of numerous diseases, including cancer. For 2D, cell movement starts with protrusion of the cell membrane followed by the formation of new adhesions at the cell front that link the actin cytoskeleton to the extracellular matrix, generation of traction forces that move the cell forwards and disassembly of adhesions at the cell rear. Although valuable knowledge has been accumulated through analysis of various 2D models, some of these insights are not directly applicable to migration in 3D. In any case, all these processes are regulated by environmental signals from the surrounding microenvironment that allow cells to guide and regulate their directional movement. Unraveling the intrinsic mechanisms that cells use to define their migration is crucial for advancing in the development of new technologies in regenerative medicine and treatment of cancer. Due to the complexity of all these ...