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Creative Bioarray provides cell proliferation assay service for our customer. We are capable of performing different cell proliferation assays based on several concepts, which are measuring rate of DNA replication, analysis of metabolic activity, cell surface antigen recognitions, detecting proliferation markers, ATP measurement, measures of membrane integrity and so on.
The CyQUANT NF Cell Proliferation Assay Kit provides a fast and sensitive method for counting cells in a population and measuring proliferation in microplate format. Features of the CyQUANT NF Cell Proliferation Assay Kit: More sensitive than MTT or AlamarBlue assays Linear detection range from
... Abstract ...The cell proliferation assay is an important tool in the assessment of... Introduction ...Cell proliferation assays are employed frequently in immunological ca...,Cell,Proliferation,Assays,biological,advanced biology technology,biology laboratory technology,biology device technology,latest biology technology
BioAssay record AID 1077586 submitted by ChEMBL: Antiproliferative activity against human PLC/PRF/5 cells assessed as inhibition of cell proliferation at 10 to 100 uM by MTT dye uptake assay.
Little knockdown but big effect on proliferation - posted in siRNA, microRNA and RNAi: Hi folks,Hope you are well all !! I did knockdown lately on cell line expressed in GOI and it was tested by qPCR. The results showed that i got moderate suppression in mRNA level in my GOI, following the knockdown i did cell proliferation ( cell viability ) and the results showed that there is an effect on proliferation rate.]My question is how was an effect on proliferation when there was little...
We have shown that 4-1BB in myeloid cells, particularly in APCs, negatively regulates peripheral T cell responses in vivo. Thus, adoptively transferred CD4+ and CD8+ T cells showed the enhanced T cell proliferation in tumor-bearing RAG2−/−4-1BB−/− mice, and DCs and IL-15 were primarily responsible for this enhanced T cell proliferation. However, isolated 4-1BB+/+ and 4-1BB−/− DCs made comparable levels of IL-15, and individual 4-1BB−/− DCs induced T cell responses in vivo less efficiently than 4-1BB+/+ DCs. Therefore, we concluded that 4-1BB deficiency in myeloid cells in vivo induces the enhanced proliferation of peripheral T cells by promoting the accumulation of DCs in secondary lymphoid organs.. Although enhanced T cell responses were first reported when 4-1BB−/− mice were generated more than a decade ago (29), the underlying mechanism was not understood. Other studies have also pointed to a negative regulatory function of 4-1BB in modulating T cell responses. Thus, ...
Creative Proteomics offers sensitive, reliable, and accurate Cell Proliferation Assay via DNA Synthesis to study cell proliferation.
A serum-free or serum-depleted medium for the short- and long-term proliferation and development of cells, particularly hematopoietic cells and bone marrow stromal cells, the medium comprising cell proliferation and development effective amounts of: a standard culture medium such as Iscoves modified Dulbeccos medium; serum albumin; transferrin; a source of lipids and fatty acids; cholesterol; a reducing agent; pyruvate; a glucocorticoid (when the cells to be cultured are hematopoietic cells); nucleosides for synthesis of DNA and RNA; growth factors that stimulate the proliferation and development of stromal cells and cells from a variety of tissues or organs, such as epidermal growth factor, fibroblast growth factor, platelet derived growth factor, and insulin; and extracellular matrix materials, such as collagen, fibronectin, and laminin.
NSCLC is the most prevalent cancer types and has highest mortality rate in China [1]; however, the progression mechanisms of NSCLC have largely remained elusive. Ample evidence indicates a crucial role for miRNAs in human cancer [21], especially the miRNAs participate in the initiation, promotion, and progression of NSCLC. For instance, miR-21 promotes growth and invasion of NSCLC [22]. In addition, miR-494, miR-101, miR-1254, miR-574-5p, miR-143 and miR-181a were demonstrated to be involved in NSCLC [23-25]. In the present study, we certified that miR-361-3p was frequently down-regulated in NSCLC, and first found that the reduced miR-361-3p expression was closely related to advanced stage and lymph node metastasis of NSCLC. Furthermore, we demonstrated that overexpression of miR-361-3p could suppress NSCLC cell proliferation, migration and invasion in vitro and in vivo. The versatile functions of miR-361-3p in tumor cell proliferation, migration and invasion suggest its potential application as ...
... Quantitating cell number is more accurate using the Quantos cell...The Quantos cell proliferation assay kitprovides a simpl...Researchers are frequently interested in determining the effects of va...We set out to determine how well the Quantos cell proliferation assay ...,Cell,Proliferation,Kit,Outperforms,the,Competition,in,the,Range,of,Cells,,,Typically,Counted,biological,advanced biology technology,biology laboratory technology,biology device technology,latest biology technology
Breast cancer is one of the most lethal types of cancer in women worldwide due to the late stage detection and resistance to traditional chemotherapy. The human epidermal growth factor receptor 2 (HER2) is considered as a validated target in breast cancer therapy. Even though a substantial effort has been made to develop HER2 inhibitors, only lapatinib has been approved by the U.S. Food and Drug Administration (FDA). Side effects were observed in a majority of the patients within one year of treatment initiation. Here, we took advantage of bioinformatics tools to identify novel effective HER2 inhibitors. The structure-based virtual screening combined with ADMET (absorption, distribution, metabolism, excretion and toxicity) prediction was explored. In total, 11,247 natural compounds were screened. The top hits were evaluated by an in vitro HER2 kinase inhibition assay. The cell proliferation inhibition effect of identified inhibitors was evaluated in HER2-overexpressing SKBR3 and BT474 cell lines. We
CD44 is a causal factor for tumor invasion, metastasis and acquisition of resistance to apoptosis. CD44 knockdown using inducible short hairpin RNA (shRNA) significantly reduces cell growth and invasion. Short hairpin RNA against CD44 and pGFP-V-RS-vector was used for knockdown of CD44 expression in SW620 colon cancer cells. Cell growth, invasion and migration assay, immunofluorescence for β-catenin expression and western blotting for Wnt signaling molecules were analyzed. Cell cycle analysis and western blot analysis for apoptotic molecules were evaluated. Short hairpin RNA against CD44 reduced the expression of CD44. Cell proliferation, migration and invasion were markedly inhibited and apoptosis was increased in shRNA CD44-transfected cells. Knockdown of CD44 decreased the phosphorylation of PDK1, Akt and GSK3β, and β-catenin levels. Decreased phosphorylated Akt led to an increase in phosphorylated FoxO1 and induced cell cycle arrest in the G0-G1 phase and a decrease in the S phase. The ...
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Perifosine and CCI 779 co-operate to induce cell death and decrease proliferation in PTEN-intact and PTEN-deficient PDGF-driven murine glioblastoma.
: Migration and invasion enhancer 1 (MIEN1) is a membrane-anchored protein and exists in various cancerous tissues. However, the roles of MIEN1 in prostate cancer have not yet been clearly addressed. We determined the expression, biological functions, and regulatory mechanisms of MIEN1 in the prostate. The results of immunohistochemical analysis indicated that MIEN1 was expressed specifically in epithelial cells and significantly higher in adenocarcinoma as compared to in normal tissues. MIEN1 enhanced in vitro cell proliferation, invasion, and in vivo tumorigenesis. Meanwhile, MIEN1 attenuated cisplatin-induced apoptosis in PC-3 cells. Overexpression of NF-ĸB-inducing kinase (NIK) enhanced MIEN1 expression, while overexpression of NF-ĸB inhibitor α (IĸBα) blocked MIEN1 expression in PC-3 cells. In prostate carcinoma cells, MIEN1 provoked Akt phosphorylation; moreover, MIEN1 downregulated N-myc downstream regulated 1 (NDRG1) but upregulated interleukin-6 (IL-6) gene expression. MK2206, an
ATCC Cell Proliferation Assay kits are convenient and valuable tools for the quantitative evaluation of a cell populations response to external factors that affect cell viability and growth.
Probable proto-oncogene that regulates cell proliferation, growth, migration and epithelial to mesenchymal transition. Through the degradation of FBXW7, may act indirectly on the expression and downstream signaling of MTOR, JUN and MYC (PubMed:24344117). May play also a role in cell proliferation through activation of the ERK1/ERK2 signaling cascade (PubMed:25646692). May also be important for proper chromosome congression and alignment during mitosis through its interaction with KIF22 ...
Gentaur molecular products has all kinds of products like :search , Trevigen \ MTT Cell Proliferation Assay Kit \ 4890-25-K for more molecular products just contact us
Effect of GPC3 on cell proliferation and clonogenic capacity of liver CD90+GPC3+CSCs.(A) Cell proliferation was assessed after GPC3 knockdown in PLC CD90+GPC3+
A colorimetric cell proliferation assay using soluble tetrazolium sodium [(CellTiter 96? Aqueous One Remedy) cell proliferation reagent, comprising the (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt) and an electron coupling reagent phenazine ethosulfate], was optimized and certified for quantitative dedication of IL-15 dependent CTLL-2 cell proliferation activity. of scripts written in the R Statistical Language and Environment utilizing a […]. ...
We report a novel mechanism of cellular growth control. Increasing the density of endothelial or smooth muscle cells in culture increased cell-cell contact and decreased cell spreading, leading to growth arrest. Using a new method to independently control cell-cell contact and cell spreading, we fou …
Introduction The difficulty in re-growing and mineralizing new bone after severe fracture can result in loss of ambulation or limb. Here we describe the sequential roles of FGF-2 in inducing gene expression, cell growth and BMP-2 in gene expression and mineralization of bone. Materials and methods The regulation of gene expression was determined using real-time RTPCR (qRTPCR) and cell proliferation was measured by thymidine incorporation or fluorescent analysis of DNA content in MC3T3E1 osteoblast-like cells. Photomicroscopy was used to identify newly mineralized tissue and fluorescence was used to quantify mineralization. Results Fibroblast growth factor-2 (FGF-2) had the greatest ability to induce proliferation after 24 hours of treatment when compared to transforming growth factor beta (TGFβ, insulin-like growth factor-1 (IGF-1), bone morphogenic protein (BMP-2), platelet derived growth factor (PDGF) or prostaglandin E2 (PGE2). We found that FGF-2 caused the most significant induction of ...
Cell proliferation assays are performed by four decades in cancer research to test the anti-proliferative activity of natural products and synthetic compounds in in vitro tumor models such as cell lines. However, current parameters used to quantify growth inhibition lead to a misinterpretation of results based on the exponential, and not linear, proliferation of cells in culture. We recently published in Journal of Cellular Physiology the development and experimental validation of a new parameter for the analysis of growth inhibition in proliferation assays, termed relative doubling capacity, that can be used to properly quantify the anti-proliferative activity of tested compounds in cell cultures and compare drug efficacy between distinct cell models. ...
[109 Pages Report] Check for Discount on Global Cell Proliferation Kit Sales Market Report 2017 report by QYResearch Group. In this report, the global Cell Proliferation Kit market is...
Definition of Cell proliferation with photos and pictures, translations, sample usage, and additional links for more information.
Figure 1: Effects of PKR on the proliferation and translation. (a) Effects of PKR on the proliferation of HeLa cells. After being transfected with plasmids PKR, PKR siRNA, or GFP, HeLa cells were plated in multiple wells of a 96-well plate and grown for 24 hr for cell proliferation assays. Cells from the sample preparations were collected for immunoblotting. Proliferation rate of the control sample was normalized to 100%. PKR, WT PKR; si-PKR, PKR siRNA; Ctrl, GFP. Upper panel, averaged data (N=4 ...
The master regulator p53 is a prominent tumor suppressor gene, functioning in the cell as a tetrameric (dimer of dimers) sequence-specific transcription factor, able to bind to two copies of a decameric sequence with the RRRCWWGYYY consensus (where R stands for a purine, W for A/T and Y for a pyrimidine) representing the so called p53-response element (p53-RE) [1]. p53 is known to be inducible in response to a large number of cellular stress signals that, besides genotoxic stress, include carbon and oxygen deficiencies, perturbations of the translation apparatus, excessive proliferation signals, alteration in microtubule dynamics [2, 3]. There are ,100 established p53 targets genes that link p53 to cell cycle arrest, apoptosis, DNA repair and inhibition of angiogenesis [3-6]. More recently, p53 was demonstrated to modulate the expression of genes able to modify glucose as well as lipid metabolism, induction of autophagy, immune responses and cell motility [7-11].. A direct role of p53 on the ...
Cell proliferation analyses are crucial for cell growth and differentiation studies, and are often used to evaluate both compound toxicity and inhibition of tumor cell growth during drug development. Proliferation measurements are typically based on average DNA content or cellular metabolism, or they quantify DNA synthesis.
Find and order buffers and products like this Ready-to-use Cell Proliferation Colorimetric Reagent, WST-1 on www.antibodies-onli... | Order product ABIN1304384.
Abstract: miRNA-221 was a carcinogenic factor in many cancers, however, it is limited that the correlation between miRNA-221 and progression of cervical cancer. So we here aimed to determine the function of miRNA-221 in cervical cancer proliferation and a
Concurrent in vivo proliferation and CTL activity by gB-specific CD8+ T cells in the PLNs after cutaneous infection with HSV-1. (A) CFSE-labeled lymph node cell
To determine the effect of protein treatments in cell proliferation, MDA-MB-231 breast cancer cells were first injected into the mammary fat pad of nude mice, and when tumors grew to 10 mm in diameter, mice were treated once only with purified Endo (20 mg/kg), CD (40 mg/kg), or EndoCD (60 mg/kg) proteins plus 500 mg/kg 5-FC, a clinically sufficient dose of 5-FU (15 mg/kg; 1× 5-FU), or 10 times the clinically sufficient dose (150 mg/kg; 10× 5-FU). The choice of 20 mg/kg Endo was based on a previous preclinical study (15) and is also within the dose tested in the phase I clinical trial (ref. 18; 15-600 mg/m2 in human is equivalent to 4.8-194.4 mg/kg in mouse; ref. 30). Tumors were harvested from mice 48 hours after treatment and labeled with bromodeoxyuridine (BrdU) antibody for in vivo BrdU incorporation analysis. The results show that EndoCD/5-FC most significantly reduced cancer cell proliferation (Fig. 2B) compared with all other treatment groups.. The potent inhibitory activity of ...
Trouvez tous les livres de Lam, Eric W-F - Phosphoinositide 3-Kinase Signalling Pathway: The Key to Cell Proliferation and Death. Sur eurolivre.fr,vous pouvez commander des livres anciens et neufs.COMPARER ET acheter IMMÉDIATEMENT au meilleur prix. 9781860946264
This inhibition concerns cell proliferation and the expression of IL-8, u-PA, and MMP - 9, which can AZD0530 proposes inhibit invasion of cancer cells in the
Gen5 allows measuring cell proliferation as both an end point and kinetic imaging assay and can be run with temperature and gas control.
A method for treating a disorder characterized by excessive cell proliferation in a patient by administering to the patient a therapeutically effective amount of sclareolide.
cell proliferation - Read articles from Issue 2009(04). Read article PDFs using your inistitutions subscriptions with no additional login.
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Liu, X., Go, M.-L. (2006-01-01). Antiproliferative properties of piperidinylchalcones. Bioorganic and Medicinal Chemistry 14 (1) : 153-163. [email protected] Repository. https://doi.org/10.1016/j.bmc.2005.08. ...
I do a proliferation assay after pulsing PBMCS with CFSE (5micromol for 2-10million cells) and then staining with CD3. I sort the cells and then stimulate them for proliferation with PHA(2microlitre). I also stain the cells with CD4 and CD8 on the day of analysis. I add PI jus before running the cells on the flow cytometer to discriminate for live vs dead cells.I am worried because I only get a single peak for each day (1-5 days expt). am i using too much CFSE? is that making it difficult to discern the peaks? Can somebody help with the trouble shooting. I also apply single compensation controls for the first day and find no spill for the rest of the days by using the same settings ...
I do a proliferation assay after pulsing PBMCS with CFSE (5micromol for 2-10million cells) and then staining with CD3. I sort the cells and then stimulate them for proliferation with PHA(2microlitre). I also stain the cells with CD4 and CD8 on the day of analysis. I add PI jus before running the cells on the flow cytometer to discriminate for live vs dead cells.I am worried because I only get a single peak for each day (1-5 days expt). am i using too much CFSE? is that making it difficult to discern the peaks? Can somebody help with the trouble shooting. I also apply single compensation controls for the first day and find no spill for the rest of the days by using the same settings ...
Cell labeling probes (both antibodies and non- antibodies) can be used in a number of applications, including cell cycle, apoptosis, viability, cell proliferation, cell movement. Check out our upgraded Cell Health and Proliferation webpage to learn more about how these reagents work and how they can aid you.
Cell labeling probes (both antibodies and non- antibodies) can be used in a number of applications, including cell cycle, apoptosis, viability, cell proliferation, cell movement. Check out our upgraded Cell Health and Proliferation webpage to learn more about how these reagents work and how they can aid you.
A proliferation in protected cell company (PCC) structures being experienced around the world was a key factor in White Rock setting up another operation.
J:171486 Rutter M, Wang J, Huang Z, Kuliszewski M, Post M, Gli2 influences proliferation in the developing lung through regulation of cyclin expression. Am J Respir Cell Mol Biol. 2010 May;42(5):615-25 ...
Dr. Kendall Smith, the Rochelle Belfer Professor of Immunology and Medicine at Weill Cornell Medical College, reviews the progress that has been made in the past 50 years in our understanding of the molecular control and regulation of normal cell proliferation, and how this understanding has led for the first time to a new insight into the molecular pathogenesis of abnormalities of cellular growth regulation, a.k.a. cancer.
Large variations in MTT - posted in MTT, Proliferation and Cytotoxicity Assay: Control (Sample 1) 0.331 , 0.333 (Sample 2)0.457, 0.454 (Sample 3)0.450, 0.451 Treatment 1 (Sample 1) 0.390 , 0.374 (Sample 2)0.439, 0.458 (Sample 3)0.441, 0.444 Treatment 2 (Sample 1) 0.418 , 0.424 (Sample 2)0.446, 0.471 (Sample 3)0.406, 0.436 + Control (Sample 1) 0.428 , 0.454 (Sample 2)0.429, 0.432 (Sample 3)0.441, 0.427 My cells are adherent cancer cells, seeded in 24-wells at 2500 cells/well and harvested...
Contrary to previous findings suggesting a protein measures cell length, a different protein is found to measure the cells surface area.
Receive a complimentary sample of NeuroCult™ NS-A Proliferation Kit (Human). Just fill out the form and a representative will contact you to arrange the sample.
A protein called CDKG1 is analogous to a human protein called CDK4/6 that stimulates cell proliferation and whose activity is frequently misregulated in cancer.
Our results are consistent with previous studies in that proliferative responses are primarily mediated by E2F1, E2F2 and E2F3, whereas the recruitment of E2F4 on the promoters suppresses cell proliferation [31], [32], [38 ...
ISBN 978-0-9809667-5-6 1. Cells--Growth--Mathematical models. 2. Cell proliferation Mathematical models. 3. Cells--Mechanical properties--Mathematical models. 4. Cell division--Mathematical models. 5. Growth--Regulation--Mathematical models. I. Title. QH511.S55 2010 571.849 C2010-900110-9 ...
Full Text - Inducing cardiomyocyte proliferation is a hopeful approach for cardiac regeneration following myocardial infarction. Previous studies have shown that p21 inhibits the cardiomyocyte proliferation and cardiac regeneration. Deacetylation of p21 by Sirt1 deacetylase may reduce p21 abundance and remove p21-induced cell cycle arrest. However, whether p21 deacetylation and Sirt1 deacetylate control cardiomyocyte proliferation is unclear. Here, we show that acetylation of p21 induces cardiomyocyte proliferation arrest, whereas blocking the acetylation of p21 increases cardiomyocyte proliferation. P21 can be acetylated by Sirt1, and Sirt1 activate p21 ubiquitination through deacetylation. Additionally, overexpression of Sirt1 induces EdU-, pH3-, and Aurora B-positive cardiomyocytes in neonatal and adult mice. In contrast, depletion of Sirt1 reduces cardiomyocyte proliferation in vitro and in vivo. Moreover, Sirt1 protects cardiac function, reduces cardiac remodeling, inhibits
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 ...
Markers of crypt cell proliferation are frequently employed in studies of the impact of genetic and exogenous factors on human colonic physiology. Human studies often rely on the assessment of tissue acquired at endoscopy. Modulation of cell proliferation by bowel preparation with oral laxatives may confound the findings of such studies, but there is little data on the impact of commonly used bowel preparations on markers of cell proliferation. Crypt length, crypt cellularity and crypt cell proliferation were assessed in biopsies acquired after preparation with either Klean-Prep or Picolax. Crypt cell proliferation was assessed by whole-mount mitotic figure count, and by two different immunohistochemical (IHC) labelling methods (Ki-67 and pHH3). Subsequent biopsies were obtained from the same patients without bowel preparation and similarly assessed. Parameters were compared between groups using analysis of variance and paired t-tests. There were significant differences in labelling indices (LI) between
The immediate goal of this work was to construct a computable network model for cell proliferation in non-diseased lung. Lung epithelial cells are stimulated to proliferate upon injury as a mechanism for renewal [1]. Alterations in the control of cell proliferation play a pivotal role in lung diseases including cancer, COPD, and pulmonary fibrosis. Cancer results from both gains of inappropriate growth signaling as well as the loss of mechanisms inhibiting proliferation [2]. Hyperplasia of mucus-producing goblet cells and airway smooth muscle contribute to COPD pathology [3]. Pulmonary fibrosis is characterized by excessive proliferation of lung fibroblasts, resulting in impaired lung function [4]. Thus, increasing the molecular understanding of the regulation of cell proliferation in the lung will serve to aid in the treatment and prevention of several lung diseases.. Comprehensive and detailed pathway or network models of the processes that contribute to lung disease pathology are needed to ...
Regulation of mRNAs is one way to control protein levels and thereby important cellular processes such as growth, invasion and apoptosis. G3BPs constitute a family of mRNA-binding proteins, shown to be overexpressed in several cancer types, including breast, colon and pancreas cancer. G3BP has been reported to both stabilize and induce degradation of specific mRNAs. Here, we show that G3BP1, but not G3BP2, supports proliferation of several breast cancer cell lines. Global gene expression analyses of G3BP1- and G3BP2-depleted cells indicate that primarily G3BP1, and much less G3BP2, influences mRNA expression levels. Peripheral myelin protein 22 (PMP22) was one gene that was significantly influenced by G3BP1 depletion which led to a 2-3 fold increased expression. Depletion of PMP22 resulted in increased proliferation and the G3BP1-mediated effect on proliferation was not seen upon PMP22-depletion. This indicates a novel role for G3BP1 in the regulation of cell proliferation in breast cancer cells,
Determination of apoptosis, proliferation status and [O.sup.6]-methylguanine DNA methyltransferase methylation profiles in different immunophenotypic profiles of diffuse large B-cell lymphoma / Diffuz buyuk B-hucreli lenfomanin forkli immunofenotipik profillerinde apoptozis, proliferasyon durumu ve [O.sup.6]-metilguanin DNA metiltransferaz metilasyon profillerinin tespiti.
Various assays, using different strategies, are available for assessing cultured cell proliferation. These include measurement of metabolic activity (tetrazolium salts and alamarBlue), DNA quantification using fluorophores (Hoechst 33258 and PicoGreen), uptake of radioactively-labeled DNA precursors such as [3H]thymidine, and physical counting (hemocytometer). These assays are well established in characterizing cell proliferation in two-dimensional (2D), monolayer cultures of low cell densities. However, increasing interest in 3D cultures has prompted the need to evaluate the effectiveness of using these assays in high cell density or 3D cultures. We show here that typical cell proliferation assays do not necessarily correlate linearly with increasing cell densities or between 2D and 3D cultures, and are either not suitable or only rough approximations in quantifying actual cell numbers in a culture. Prudent choice of techniques and careful interpretation of data are therefore recommended when ...
Resveratrol is the subject of intense research because of the abundance of this compound in the human diet and as one of the most valuable natural chemopreventive agents. Further advances require new resveratrol analogs be used to identify the struct
TY - JOUR. T1 - Conflicting evidence for the role of JNK as a target in breast cancer cell proliferation. T2 - comparisons between pharmacological inhibition and selective shRNA knockdown approaches. AU - Wood, Rachel A.. AU - Barbour, Mark J.. AU - Gould, Gwyn W.. AU - Cunningham, Margaret R.. AU - Plevin, Robin J.. N1 - © 2017 The Authors. Pharmacology Research & Perspectives published by John Wiley & Sons Ltd, British Pharmacological Society and American Society for Pharmacology and Experimental Therapeutics.. PY - 2018/2/28. Y1 - 2018/2/28. N2 - As a target, the JNK pathway has been implicated in roles including cell death, proliferation, and inflammation in variety of contexts which span cardiovascular disease, neurodegenerative pathologies, and cancer. JNK1 and JNK2 have recently been demonstrated to function independently, highlighting a new parameter in the study of the JNK pathway. In order for JNK1 and JNK2-specific roles to be defined, better tools need to be employed. Previous ...
Accumulating studies have focused on the role of miRNAs play in regulating cell proliferation process in gastric cancer. MiR-29c has been shown to be down-regulated in gastric cancer, but the downstream targets differ and it is not clear how miR-29c mediates cell responses in varying cell contexts. Han et al. reported that miR-29c involved in the initiation of gastric carcinogenesis by directly targeting ITGB1 [12]. They found restoration of miR-29c inhibits cell proliferation, adhesion, invasion and migration in gastric cancer. Another research group verified the downregulation of miR-29c in gastric cancer patients and assessed proliferation and colony formation ability of miR-29c by targeting RCC2 [13]. It was showed that all the members of miR-29 family were down-regulated in gastric cancer and miR-29c was more significant as a signature miRNA than miR-29a or 29b for gastric cancer. Furthermore, they demonstrated that miR-29 family directly targeted CCND2 and MMP2 to influence gastric cancer ...
F the soft agar colony formation in comparison with vector control cells exposed to arsenite for eight weeks. A single explanation of these information is the
Measurement of cell proliferation is necessary for testing the effects of pharmacological agents or growth factors, assessing cytotoxicity or investigating circumstances of cell activation. In a cell proliferation assay, the increase in number of cells or change in the proportion of cells that is dividing is assessed. Trevigen® offers a Calcein-AM based kit to determine cell viability as well as the tetrazolium salts MTT and XTT metabolic cell proliferation assay kits.. ...
This paper represents a study on the effect of electrical pulses on adult stem cells, especially on proliferation control and also as a method of deliverin
I am doing TCR transgenic T cell proliferation assay in vitro. (OT-I CD8 T cells and DO.11 CD4 T cells). There are three questions: 1. For 96-well plate, how many T cell should be used in each well? I used 200,000 cells/well, is that too high? And after how many days coculture with APC should H3 thymidine be added? 2. Which medium is good for the assay? I only used RPMI, any one has better experience with other medium? 3. Does it make difference to use mouse serum v.s. FCS? What percentage of serum should be added to the medium? Thanks for help. Kang e-mail: Liuk at rockvax.rockefeller.edu ...
TY - JOUR. T1 - Tumor growth dynamics with nutrient limitation and cell proliferation time delay. AU - Alsheri, Ahuod. AU - Alzahrani, Ebraheem O.. AU - Asiri, Asim. AU - El-Dessoky, Mohamed M.. AU - Kuang, Yang. PY - 2017/12/1. Y1 - 2017/12/1. N2 - It is known that avascular spherical solid tumors grow monotonically, often tends to a limiting final size. This is repeatedly confirmed by various mathematical models consisting of mostly ordinary differential equations. However, cell growth is limited by nutrient and its proliferation incurs a time delay. In this paper, we formulate a nutrient limited compartmental model of avascular spherical solid tumor growth with cell proliferation time delay and study its limiting dynamics. The nutrient is assumed to enter the tumor proportional to its surface area. This model is a modification of a recent model which is built on a two-compartment model of cancer cell growth with transitions between proliferating and quiescent cells. Due to the limitation of ...
The Wnt signal pathway is composed of β-catenin and transcriptional factor TCF-4 (2 , 3 , 19, 20, 21) . These factors activate the target genes that preserve the consensus motif (A/TA/TCAAAG) for TCF-4 binding in the promoter region (6) . Recent studies have shown that cyclin D1, c-myc, MMP7, and c-jun could be target genes for the Wnt signal pathway (7, 8, 9, 10) . Therefore, Wnt signal may induce cell proliferation through activation of these target genes (22, 23, 24, 25) . To our knowledge, there is no report on RCCs regarding the significance of the Wnt signal factors in cell proliferation and/or apoptosis through regulation of downstream target genes. In this study, we evaluated the significance of the Wnt signal pathway in RCC through the analysis of cyclin D1, c-myc, MMP7, and c-jun in relation to β-catenin and TCF-4 alterations.. TCF-4 expression has been intensively investigated in the epithelium of the gastrointestinal tract (26 , 27) , and the presence of splicing isoforms in TCF-4 ...
Lack of IGF2 in mice results in diminished embryonic growth due to diminished cell proliferation. Here we show that mouse embryonic fibroblasts lacking the RNA-binding protein IMP1 (IGF2 mRNA-binding protein 1) have defective splicing and translation of IGF2 mRNAs, markedly reduced IGF2 polypeptide production, and diminished proliferation. The proliferation of the IMP1-null fibroblasts can be restored to wild-type levels by IGF2 in vitro or by re-expression of IMP1, which corrects the defects in IGF2 RNA splicing and translation. The ability of IMP1 to correct these defects is dependent on IMP1 phosphorylation at Ser181, which is catalyzed cotranslationally by mTOR complex 2 (mTORC2). Phosphorylation strongly enhances IMP1 binding to the IGF2-leader 3 5 untranslated region, which is absolutely required to enable IGF2-leader 3 mRNA translational initiation by internal ribosomal entry. These findings uncover a new mechanism by which mTOR regulates organismal growth by promoting IGF2 production in ...
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Visit CellSignal.com to view our Cellular Assay Kits materials including Cell Proliferation Assays & more. CST - Customer satisfaction is our highest priority.
Visit CellSignal.com to view our Cellular Assay Kits materials including Cell Proliferation Assays & more. CST - Customer satisfaction is our highest priority.
Fibulins not only function as molecular bridges within the cellular microenvironment but also influence cell behavior. Thus, fibulins may contribute to create a permissive microenvironment for tumor growth but can also stimulate different mechanisms that may impede tumor progression. This is the case with Fibulin-5, which has been shown to display both tumor-promoting and tumor-protective functions by mechanisms that are not totally defined. We show new evidence on the tumor-protective functions displayed by Fibulin-5 in MCF-7, T47D and MDA-MB-231 breast cancer cells including the inhibition of invasion and proliferation capacity and hampering the ability to form mammospheres. Reduction in the level of phosphorylation of Ser residues involved in the nuclear translocation of β-catenin may underlie these antitumor effects. We also found that Fibulin-5 reduces the level of expression of Ki-67, a nuclear protein associated with cell proliferation. Moreover, reduction in Fibulin-5 expression ...
The present study, to the best of the authors knowledge, demonstrated for the first time, that miR-614 was upregulated in OC clinical tissues and cells. Increased expression of miR-614 led to the promotion of cell proliferation and colony-forming abilities, and conversely, decreased the apoptotic rate of OC cells. Additionally, PPP2R2A may act as a novel target of miR-614. The present study indicated that miR-614 may act as a novel tumor promoter in OC by targeting PPP2R2A.. Accumulating evidence suggests that miRNAs exhibit an essential role in human cancer pathological proceedings via controlling different target genes, including those involved in cell proliferation, migration, invasion, cycle and apoptosis (15-18). Dysregulation of miRNA frequently occurs in novel types of cancers, including ovarian cancer. miR-21-3p inhibits cell proliferation and invasion of ovarian cancer by targeting RNA binding protein with multiple splicing, RCC1 and BTB domain containing protein 1 and Zinc finger ...
miRNAs are emerging as critical regulators in carcinogenesis and tumor progression. Recently, microRNA-122 (miR-122) has been proved to play an important role in hepatocellular carcinoma, but its functions in the context of breast cancer (BC) remain unknown. In this study, we report that miR-122 is commonly downregulated in BC specimens and BC cell lines with important functional consequences. Overexpression of miR-122 not only dramatically suppressed cell proliferation, colony formation by inducing G1-phase cell-cycle arrest in vitro, but also reduced tumorigenicity in vivo. We then screened and identified a novel miR-122 target, insulin-like growth factor 1 receptor (IGF1R), and it was further confirmed by luciferase assay. Overexpression of miR-122 would specifically and markedly reduce its expression. Similar to the restoring miR-122 expression, IGF1R downregulation suppressed cell growth and cell-cycle progression, whereas IGF1R overexpression rescued the suppressive effect of miR-122. To identify
Nervous system development requires balance between the regeneration of neural progenitor cells (NPCs) through proliferation and the specification and differentiation of NPCs, and this balance is likely controlled by both intrinsic and extrinsic pathways. Premature differentiation or excessive proliferation of the NPCs results in aberrant tissue development. Jo et al. used the mouse retina as a model to study the effect of loss of function of the lipid and protein phosphatase Pten, which results in excessive activation of the kinase Akt. Postmitotic retinal neurons showed enhanced phosphorylation (activation) of Akt compared with retinal progenitor cells (RPCs). Targeted deletion of Pten in distal RPCs (and the cells that differentiate from these progenitors) (Pten-cko) resulted in a larger region of Pten-cko cells in the embryonic retina than was predicted and was associated with reduced numbers of apoptotic cells and increased numbers of proliferating cells in the embryonic retina, suggesting ...
Both cell proliferation and cell size control are fundamental biological processes that must be carefully orchestrated, and dysregulation of either can lead to diseases such as cancer. In contrast to our understanding of the mechanisms that control cell proliferation, less is known about the mechanisms that control cell size and, particularly, the mechanisms by which cell proliferation and cell size are coordinately regulated. Recently, we identified a novel protein named FIP200, which plays an important role in the regulation of cell cycle progression (Abbi et al., 2002). In this study, we showed that FIP200 can also regulate cell size through interaction with the TSC1-TSC2 complex and activation of S6K. These results identify FIP200 as a regulator that plays roles in both cell proliferation and cell size control.. Most other proteins known to play roles in both cell proliferation and cell size usually regulate these two cellular processes in a similar manner. For example, PTEN can inhibit cell ...
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Ng F, Ye J, et al. PERK promotes cancer cell proliferation and tumor development by limiting oxidative DNA harm. Oncogene 29: 38813895. 42. Min L, Ji Y, Bakiri
Supervisor: Golnar Kolahgar. The intestinal epithelium constantly regenerates from stem cells, which adjust their behaviour to the changing physiological conditions the gut is exposed to. For example, stem cell proliferation rates can transiently increase to speed up regeneration after tissue loss or in response to the diet, before reverting to steady-state levels once correct tissue size is reached. This plasticity is essential for intestinal function, as lack of regeneration causes tissue atrophy whereas unrestricted stem cell proliferation promotes cancer. We use the genetically tractable Drosophila gut to identify the secreted and physical factors regulating gut plasticity. In particular, we use targeted genetic screens and functional analyses, to identify novel extracellular signalling molecules regulating cell proliferation in contexts that trigger reversible changes in gut size. As the regulation of intestinal proliferation is largely conserved between Drosophila and mammals this work has ...
Reduction of Prep1 Levels Affects Differentiation of Normal and Malignant B Cells and Accelerates Myc Driven Lymphomagenesis. . 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.
The intermediate-conductance Ca2+-activated K+ channel KCa3.1 is widely expressed in cells of the immune system such as T- and B-lymphocytes, mast cells, macrophages and microglia, but also found in dedifferentiated vascular smooth muscle cells, fibroblasts and many cancer cells including pancreatic, prostate, leukemia and glioblastoma. In all these cell types KCa3.1 plays an important role in cellular activation, migration and proliferation by regulating membrane potential and Ca2+ signaling. KCa3.1 therefore constitutes an attractive therapeutic target for diseases involving excessive proliferation or activation of one more of these cell types and researchers both in academia and in the pharmaceutical industry have developed several potent and selective small molecule inhibitors of KCa3 ...
The application discloses novel 2-alkoxyestradiol analogs which exhibit anti-proliferative properties, and methods of making and using such compounds to inhibit undesired cell proliferation and tumor growth. Additionally, methods are disclosed of treating diseases associated with undesired angiogenesis and undesired proliferation, and methods of treating infectious disease wherein the infectious agent is particularly susceptible to inhibition by agents that disrupt microtubule organization and function.
To test if EZH2 and EED are essential for proliferation, double stranded RNA interfering oligonucleotides (siRNA oligos) were designed for both EZH2 and EED. As shown in Figure 3A, siRNA to EZH2 specifically prevented EZH2 synthesis in TIG3 diploid human fibroblasts. Almost complete depletion of both EZH2 and EED were also observed in U2OS cells (Figure 3B) and in HeLa cells (data not shown).. Cells depleted for EZH2 and EED appeared larger than control transfected cells with a senescent‐like phenotype. Inspection of transfected cultures indicated that lack of EZH2 and EED resulted in less proliferation (Figure 3C). This effect was quantified by measuring the proliferation rate of the transfected cells (Figure 3D). A decrease in either EZH2 or EED expression resulted in a strong inhibition of cell proliferation in U2OS cells. Similar reductions in growth rates were also observed in other transformed cells such as HeLa and SAOS2, as well as in the diploid fibroblasts TIG3, WI38 and HEL299 (data ...
目的:探讨反义脱氧寡核苷酸封闭HSP70基因对体外宫颈癌 HeLa 细胞增殖、凋亡及化疗敏感性的影响。方法:1)将体外培养的宫颈癌 HeLa 细胞分为正常对照组(Ctrl组)、反义寡核苷酸处理组(AS组)、正义寡核苷酸处理组(S组)、随机寡核苷酸处理组(R组),每组各5例,分别转染体外培养的宫颈癌 HeLa 细胞,采用Western免疫印迹检测各组细胞HSP70蛋白表达。2)将顺铂处理体外培养的宫颈癌 HeLa 细胞分为正常对照组(Ctrl组)、单纯顺铂处理组(Cis组)、反义寡核苷酸+顺铂处理组(AS +Cis组)、正义寡核苷酸+顺铂处理组(S +Cis组)、随机寡核苷酸+顺铂处理组 (R +Cis组),每组各8例。采用四甲基偶氮唑蓝光吸收法(methyl thiazolyl tetrazolium,MTT) 法检测 HeLa 细胞的生长抑制率; 流式细胞术检测 HeLa 细胞的凋亡率。结果:1)Ctrl组、AS组、S组、R组HSP70灰度比值分别为1.365±0.187,0.379±0.134,1.403±0.163和1.410±0
Oncotarget | https://doi.org/10.18632/oncotarget.26824 Francisca Guardiola-Serrano, Roberto Beteta-Göbel, Raquel Rodríguez-Lorca, Maitane Ibarguren, David J. López, Silvia Terés, María Alonso-Sande, Mónica...
Cancer cells demand large nutrient supplies and thus reprogram their metabolic pathways to ensure metabolic flexibility, cellular homeostasis, energy production, cell proliferation, and survival. In addition to direct modulation of signal transduction pathways causing oncogenic addiction, alterations in oncogenes also contribute to metabolic rewiring in cancer cells, resulting in the promotion of cancer cell proliferation, survival, and metastatic dissemination. Accordingly, metabolic reprogramming is now considered an important characteristic of several types of cancer, including NSCLC. Despite several ongoing approaches to target cancer metabolism, metabolic reprogramming should be therapeutically explored in additional studies. In addition, the influence of metabolic rewiring on the interaction between cancer cells and the tumor microenvironment needs to be extensively investigated to comprehensively understand the course of cancer development and progression, providing mechanistic insights ...
BioAssay record AID 217174 submitted by ChEMBL: In vitro cytotoxicity expressed as conc. that inhibits 50% of VERO(monkey kidney) cell proliferation.
The goal of this project is to describe systemic regulators of cell proliferation during cell turnover and tumorigenesis. The ideal cancer therapy aims at elimi...
Cripto-1 (CR-1) is a member of the epidermal growth factor-Cripto-1/FRL1/Cryptic gene family that plays a key role in thevarious malignant cancers. However, the role of CR-1 in prostate carcinoma (PCa) remains limited. The expression of CR-1was down-regulated by small interfering RNA (siRNA). Western blot measured the expression levels of CR-1 and somerelated proteins. We performed Cell Counting Kit-8, 5-ethynyl-2-deoxyuridine (EdU) incorporation assay and flowcytometry to detect the cellular proliferation and cycle. The transwell assay was used to observe cellular migration andinvasion. The ability of angiogenesis was evaluated by tube formation assay. Our results showed that CR-1 knockdownmarkedly inhibited cell proliferation and induced cycle arrest in G1 phase, as p21 and p27 were up-regulated, whereascyclin D1 and cyclin E1 were diminished. Moreover, silencing of CR-1 dramatically inhibited cell migration and invasion,repressed matrix metalloproteinases, and disturbed epithelial-mesenchymal ...
TY - JOUR. T1 - Signaling networks that link cell proliferation and cell fate. AU - Sears, Rosalie. AU - Nevins, Joseph R.. PY - 2002/4/5. Y1 - 2002/4/5. UR - http://www.scopus.com/inward/record.url?scp=0037023755&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0037023755&partnerID=8YFLogxK. U2 - 10.1074/jbc.R100063200. DO - 10.1074/jbc.R100063200. M3 - Article. C2 - 11805123. AN - SCOPUS:0037023755. VL - 277. SP - 11617. EP - 11620. JO - Journal of Biological Chemistry. JF - Journal of Biological Chemistry. SN - 0021-9258. IS - 14. ER - ...
Define myeloproliferative: of, relating to, or being a disorder (such as leukemia) marked by excessive proliferation of bone marrow elements and…
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Abstract Certain changes in cellular function are characteristic of renal disease. Foremost among these is the excessive proliferation of cells, but other phenotypic changes includ..
TY - JOUR. T1 - Naphthalene diimide-derivatives G-quadruplex ligands induce cell proliferation inhibition, mild telomeric dysfunction and cell cycle perturbation in U251MG glioma cells. AU - Muoio, Daniela. AU - Berardinelli, Francesco. AU - Leone, Stefano. AU - Coluzzi, Elisa. AU - di Masi, Alessandra. AU - Doria, Filippo. AU - Freccero, Mauro. AU - Sgura, Antonella. AU - Folini, Marco. AU - Antoccia, Antonio. N1 - © 2018 Federation of European Biochemical Societies.. PY - 2018/10. Y1 - 2018/10. N2 - In the present paper, the biological effects of three different naphthalene diimides (NDIs) G-quadruplex (G4) ligands (H-NDI-Tyr, H-NDI-NMe2, and tetra-NDI-NMe2) were comparatively evaluated to those exerted by RHPS4, a well-characterized telomeric G4-ligand, in an in vitro model of glioblastoma. Data indicated that NDIs were very effective in blocking cell proliferation at nanomolar concentrations, although displaying a lower specificity for telomere targeting compared to RHPS4. In addition, ...
TY - JOUR. T1 - Akt- and CREB-mediated prostate cancer cell proliferation inhibition by nexrutine, a Phellodendron amurense extract. AU - Garcia, Gretchen E.. AU - Nicole, Arevalo. AU - Bhaskaran, Shylesh. AU - Gupta, Ashima. AU - Kyprianouy, Natasha. AU - Kumar, Addanki P.. PY - 2006/1/1. Y1 - 2006/1/1. N2 - Evidence from epidemiological studies suggests that plant-based diets can reduce the risk of prostate cancer. However, very little information is available concerning the use of botanicals in preventing prostate cancer. As a first step toward developing botanicals as prostate cancer preventives, we examined the effect of Nexrutine on human prostate cancer cells. Nexrutine is a herbal extract developed from Phellodendron amurense. Phellodendron extracts have been used traditionally in Chinese medicine for hundreds of years as an anti-diarrheal, astringent, and anti-inflammatory agent. The present study investigated its potential antitumor effect on human prostate cancer cells.Our results ...
TY - JOUR. T1 - PTH-related protein enhances LoVo colon cancer cell proliferation, adhesion, and integrin expression. AU - Shen, Xiaoli. AU - Falzon, Miriam. PY - 2005/2/15. Y1 - 2005/2/15. N2 - Parathyroid hormone-related protein (PTHrP) has been localized in human colon cancer tissue and cell lines. Tumor cell adhesion to extracellular matrix (ECM) proteins plays a major role in the invasion and metastasis of tumor cells, and is mediated via integrin subunits. The LoVo human colon cancer cell line was used as a model system to study the effects of PTHrP on cell proliferation and adhesion to ECM proteins found in normal liver. Clones of LoVo cells engineered to overexpress PTHrP by stable transfection with a PTHrP cDNA showed enhanced cell proliferation vs. control (empty vector-transfected) cells. PTHrP-overexpressing cells also showed significantly higher adhesion to collagen type I, fibronectin, and laminin, and enhanced expression of the ∀2, ∀5, ∀6, ∃1 and ∃4 integrin subunits. ...
Nitric oxide (NO), which is known to inhibit systemic vascular smooth muscle cell proliferation, is used in the management of neonatal pulmonary hypertension. Our objectives were to determine: (1) if endogenous NO production by neonatal porcine pulmonary artery smooth muscle cells (PASMCs) varied with oxygen tension in vitro, and (2) the effect of exogenous NO and inducible NO synthase (iNOS) stimulators and inhibitors on PASMC proliferation and apoptosis. PASMCs were exposed to different conditions (varying PO2, NO donors and scavengers, iNOS stimulators and inhibitors) and proliferation, apoptosis, and cyclic guanosine 5-monophosphate (cGMP) assessed. PASMCs proliferated best between 5 and 10% O2 but cGMP levels were similar at all oxygen levels. NO donors (S-nitroso-N-acetyl-penicillamine, NOC-12, NOC-18) inhibited PASMC proliferation in a dose-dependent manner with associated cGMP increases, while NO scavengers (carboxy-PTIO), iNOS stimulators (interleukin-1β, lipopolysaccharide), and iNOS ...
TY - JOUR. T1 - Unusual roles of caspase-8 in triple-negative breast cancer cell line MDA-MB-231. AU - De Blasio, Anna. AU - Di Fiore, Riccardo. AU - Morreale, Marco. AU - Carlisi, Daniela. AU - Drago-Ferrante, Rosa. AU - Montalbano, Mauro. AU - Scerri, Christian. AU - Tesoriere, Giovanni. AU - Vento, Renza. PY - 2016/1/1. Y1 - 2016/1/1. N2 - Triple-negative breast cancer (TNBC) is a clinically aggressive form of breast cancer that is unresponsive to endocrine agents or trastuzumab. TNBC accounts for ∼10-20% of all breast cancer cases and represents the form with the poorest prognosis. Patients with TNBC are at higher risk of early recurrence, mainly in the lungs, brain and soft tissue, therefore, there is an urgent need for new therapies. The present study was carried out in MDA-MB-231 cells, where we assessed the role of caspase-8 (casp-8), a critical effector of death receptors, also involved in non-apoptotic functions. Analysis of casp-8 mRNA and protein levels indicated that they were ...
Two estrogen receptors (ER), ERalpha and ERbeta, are expressed in breast cancer but their role in treatment response is unclear. The overall objective of this study was to determine if the presence of ERbeta protein in breast cancer cell lines is an indicator of a poor prognosis based on cell proliferation. In addition, we determined the effect of estradiol (E2) and selective estrogen receptor modulators (SERMs), such as tamoxifen and genistein, on ERalpha and ERbeta protein regulation, to help in the understanding of the mechanism behind their role in modulating cell proliferation. Using western blot and immunofluorescence analysis, the ER positive cell lines, MCF-7 and T47D, were found to contain both ERalpha and ERbeta, and thus were used as model systems. E2 and genistein, which increased cell proliferation in both cell lines, induced an up regulation of ERbeta in both cell lines. This suggests that an estrogenic response in breast cancer cells is indicated by an increase in ERbeta ...
Background: Dentigerous cyst is the most common type of developmental odontogenic cyst which originates from REE. It has the capacity for transformation to ameloblastoma, mucoepidermoid carcinoma and squamous cell carcinoma. ki-67 and PCNA are two cell proliferation markers which can be both detected in cysts and tumors of epithelial origin. ...
There is increasing evidence for the involvement of miRNAs in mammalian biology and breast cancer. For instance, the levels of MiR-206 have been found to be higher in ERalpha-negative MB-MDA-231 cells than in ERalpha-positive MCF-7 cells [12], and enforced expression of miR-125a or miR-125b leads to coordinate suppression of ERBB2 and ERBB3 in the human breast cancer cell line SKBR3 [13]. Furthermore, MiR-27b, which is expressed in MCF-7 cells, may be one of the causes of high expression of the drug-metabolising enzyme CYP1B1 in cancerous tissues [14]. Finally, as a tumor suppressor in breast cancer cells, miR-17-5p regulates breast cancer cell proliferation by inhibiting the translation of AIB1 mRNA [15].. Research on the roles of BCSC-related miRNAs in breast cancer has great significance. Ponti [16] isolated tumorigenic breast cancer cells with stem/progenitor cell properties from a breast cancer cell line, and Huang [17] screened side population (SP) cells from a breast cancer cell line. ...