KioFuse allows you to mount remote directories into the root hierarchy of your local file system, thereby exposing KDEs advanced access capabilities (SSH, SAMBA/Windows, FTP, TAR/GZip/BZip2, WebDav, etc) to POSIX-compliant applications ...
Breast Cancer Res Treat. 2004 Jan;83(2):161-70.] Besides, I got some statements from ATCC product information sheet that most of the clusters remain in suspension until after the 2nd subculture. I found the floating MCF-7 cells alive morphology. However, I didnt collect them in subcultivation. Nevertheless, some MCF-7 cells become floating again! So I think this phenomenon is associated with adding insulin ...
Cid (36immer-Figure 6. NPY Y1R is functionally active in MCF-7 cells. Mobilization of intracellular calcium in MCF-7 (L) breast cancer cells after stimulation
Drug Deliv. 2015 May 20:1-13. Song Q, Chuan X, Chen B, He B, Zhang H, Dai W, Wang X, Zhang Q. Author information Abstract Doxorubicin (DOX) is a potent
does anyone know of any drug combinations that show synergistic effects on mcf-7, or other breat cancer cell lines? thanks!. ...
Title:Stemness Phenotype in Tamoxifen Resistant Breast Cancer Cells May be Induced by Interactions Between Receptor Tyrosine Kinases and ERα-66. VOLUME: 13 ISSUE: 3. Author(s):Leila Farahmand, Sepideh Mansouri, Narges Jafarbeik-Iravani, Azin Teymourzadeh and Keivan Majidzadeh-A*. Affiliation:Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Genetics Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran, Recombinant Proteins Department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, Tehran. Keywords:Alternative growth cascades, breast cancer, receptor tyrosine kinases, signaling pathways, stemness phenotype, tamoxifen resistance.. Abstract:Background: Tamoxifen is widely administered ...
The estrogen receptor (ER) is expressed in approximately 70% of the breast carcinomas. In general, for these patients anti-hormonal therapy is the therapy of first choice. Despite good responses in 50-60% of the patients, unfortunately all patients develop (acquired) resistance. Patients with acquired anti-hormonal resistance can be subdivided into three different groups: (1) patients that have lost ER-expression (~25%), (2) patients with preserved ER-expression (~55%) and (3) patients with enhanced ER-expression (~30%). Several studies suggest different treatment strategies for these three different ER-phenotypes in antihormonal resistant breast cancer. In patients with acquired anti-hormonal resistance, ~30% of the patients still respond to hormone-additive therapy with estrogens. In vitro studies have shown estrogen-induced apoptosis in long-treated estrogen deprived cells (simulating aromatase inhibitor resistance). It is suggested that this estrogen-hypersensitivity is accompanied by ...
Defining the molecular transcriptomic profile for predicting the clinical outcome of anthracycline resistant breast cancers. Defining metastases in relation with the primary tumor. BREAST-OMICS
Despite constituting approximately two thirds of all breast cancers, the luminal A and B tumours are poorly classified at both clinical and molecular levels. There are contradictory reports on the nature of these subtypes: some define them as intrinsic entities, others as a continuum. With the aim of addressing these uncertainties and identifying molecular signatures of patients at risk, we conducted a comprehensive transcriptomic and genomic analysis of 2,425 luminal breast cancer samples. Our results indicate that the separation between the molecular luminal A and B subtypes-per definition-is not associated with intrinsic characteristics evident in the differentiation between other subtypes. Moreover, t-SNE and MST-kNN clustering approaches based on 10,000 probes, associated with luminal tumour initiation and/or development, revealed the close connections between luminal A and B tumours, with no evidence of a clear boundary between them. Thus, we considered all luminal tumours as a single
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Aims: To unravel the cause and possible prevention of breast cancer, five potential polysaccharides from guava seed (GSPS), common buckwheat (CBPS), bitter buckwheat (B..
Surfactin has been known to inhibit proliferation and induce apoptosis in cancer cells. However, the molecular mechanisms involved in surfactin-induced apoptosis remain poorly understood. The present study was undertaken to elucidate the underlying network of signaling events in surfactin-induced apoptosis of human breast cancer MCF-7 cells. In this study, surfactin caused reactive oxygen species (ROS) generation and the surfactin-induced cell death was prevented by antioxidants N-acetylcysteine (NAC) and catalase, suggesting involvement of ROS generation in surfactin-induced cell death. Surfactin induced a sustained activation of the phosphorylation of ERK1/2 and JNK, but not p38. Moreover, surfactin-induced cell death was reversed by PD98059 (an inhibitor of ERK1/2) and SP600125 (an inhibitor of JNK), but not by SB203580 (an inhibitor of p38). However, the phosphorylation of JNK rather than ERK1/2 activation by surfactin was blocked by NAC/catalase. These results suggest that the action of ...
Recent studies have indicated a link between levels of cyclooxygenase-2 (COX-2) and development of the multidrug resistance (MDR) phenotype. The ATP-binding cassette sub-family G member 2 (ABCG2) is a major MDR-related transporter protein that is frequently overexpressed in cancer patients. In this study, we aimed to evaluate any positive correlation between COX-2 and ABCG2 gene expression using the COX-2 inducer 12-O-tetradecanoylphorbol-13-acetate (TPA) in human breast cancer cell lines. ABCG2 mRNA and protein expression was studied using real-time RT-PCR and flow cytometry, respectively. A significant increase of COX-2 mRNA expression (up to 11-fold by 4 h) was induced by TPA in MDA-MB-231 cells, this induction effect being lower in MCF-7 cells. TPA caused a considerable increase up to 9-fold in ABCG2 mRNA expression in parental MCF-7 cells, while it caused a small enhancement in ABCG2 expression up to 67 % by 4 h followed by a time-dependent decrease in ABCG2 mRNA expression in MDA-MB-231 cells.
FOXM1 is a transcription factor that coordinates expression of late cell cycle-related genes. Elevated expression of FOXM1 in breast cancer correlates with a more aggressive tumor phenotype and, as we have previously shown, is associated with resistance to endocrine treatment via 14-3-3ζ protein signaling (Bergamaschi A. et al. Breast Cancer Research 2011, 13:R7).. To better understand the role that FOXM1 plays in endocrine resistance and aggressiveness we analyzed its genome-wide DNA binding and effects on gene expression. We mapped genome-wide FOXM1 binding events, by chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq), in hormone-sensitive and resistant breast cancer cell lines after estrogen or tamoxifen treatments. We also investigated the relationship between FOXM1, estrogen receptor-α and MAPK chromatin binding events by clustering analysis of Chip-seq data and identified specific clusters of colocalized binding events as identifiers for different functional ...
The invasion-promoting effect of ET-18-OMe on MCF-7/AZ cells suggests that ET-18-OMe initiates cSrc-mediated signalling in MCF-7/AZ cells, but not in the variant MCF-7/6 cells (Figure 1). Therefore the effect of ET-18-OMe on phosphorylation of Tyr397 of FAK, the autophosphorylation site of FAK, and Tyr416 of cSrc kinase was examined. Expression levels of FAK and cSrc in both cell lines were unchanged, but kinase activity of cSrc (Figures 2A, left-hand panel and 2B) and FAK (Figures 2A, left-hand panel and 2C) were greatly enhanced in MCF-7/AZ cells 5-10 min after treatment. There was no such activation of cSrc and FAK in MCF-7/6 cells (Figure 2A, right-hand panel). The use of cSrc kinase inhibitor, PP1, blocked activation of cSrc but not Tyr397 phosphorylation on FAK, suggesting that the autophosphorylation of FAK promotes activation of cSrc. Next, the cSrc-dependent tyrosine phosphorylation sites on FAK (Tyr576, Tyr861 and Tyr925) were assayed. Time-dependent phosphorylation of FAK on Tyr925 ...
Sigma-Aldrich offers abstracts and full-text articles by [Axlund, SD; Yoo, BH; Rosen, RB; Schaack, J; Kabos, P; Labarbera, DV; Sartorius, CA].
Heres a weird one from Joseph Readys lab at UT Southwestern. Nigricanoside was isolated and reported in JACS in 2007 and was reported to be very biologically active against human breast cancer MCF-7 cells with an IC50 of 3 nM. The research lab had synthesized the molecule and found no biological activity at all, but…
The characterization of cells that have survived treatment with Adriamycin (MCF-7A), FUdR (MCF-7F), or cells that were subjected to sequential treatment with Adriamycin and FUdR (MCF-7 A/F) was performed to determine whether populations of cells surviving these treatments present different phenotypes than parental, untreated MCF-7 cells. Cells were treated with several concentrations of each of the chemotherapeutic agents. Cell populations from cultures treated with the highest concentrations of Adriamycin or FUdR, still containing viable cells after the period of treatment, were selected. The survivors of the initial Adriamycin treatment were those that remained alive after 5 days of Adriamycin treatment at a concentration of 25 ng/ml, and the survivors of the FUdR treatment were those that survived 3 days of treatment at a concentration of 10 μg/ml of FUdR. These were the highest concentrations in which cells survived, under the conditions used. The MCF-7 A/F cells were developed by treating ...
BioAssay record AID 104087 submitted by ChEMBL: In vitro inhibitory activity of compound against induced cytotoxicity in MCF-7 cell line.
Involvement of PCNK in CaMKIα phosphorylation.MCF-7 cells were transfected with siRNA targeting PNCK or control siRNA (NT1) and 72 h later, cells were exposed
Top 10 cell-lines for Q9ULL0 (Homo sapiens, UniProt): MX-1, NCI-H1963, SK-MEL-2, UACC-812, MCF-7-con, NCI-H1048, MCF-7-TP53 KD, NC-37, NALM-1, Hs 695T
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TY - JOUR. T1 - MIR-378a-3p modulates tamoxifen sensitivity in breast cancer MCF-7 cells through targeting GOLT1A. AU - Ikeda, Kazuhiro. AU - Horie-Inoue, Kuniko. AU - Ueno, Toshihide. AU - Suzuki, Takashi. AU - Sato, Wataru. AU - Shigekawa, Takashi. AU - Osaki, Akihiko. AU - Saeki, Toshiaki. AU - Berezikov, Eugene. AU - Mano, Hiroyuki. AU - Inoue, Satoshi. PY - 2015/8/10. Y1 - 2015/8/10. N2 - Breast cancer is a hormone-dependent cancer and usually treated with endocrine therapy using aromatase inhibitors or anti-estrogens such as tamoxifen. A majority of breast cancer, however, will often fail to respond to endocrine therapy. In the present study, we explored miRNAs associated with endocrine therapy resistance in breast cancer. High-throughput miRNA sequencing was performed using RNAs prepared from breast cancer MCF-7 cells and their derivative clones as endocrine therapy resistant cell models, including tamoxifen-resistant (TamR) and long-term estrogen-deprived (LTED) MCF-7 cells. Notably, ...
Signaling pathways that converge on two different transcription factor complexes, NFκB and AP-1, have been identified in estrogen receptor (ER)-positive breast cancers resistant to the antiestrogen, tamoxifen. Two cell line models of tamoxifen-resistant ER-positive breast cancer, MCF7/HER2 and BT474, showing increased AP-1 and NFκB DNA-binding and transcriptional activities, were studied to compare tamoxifen effects on NFκB and AP-1 regulated reporter genes relative to tamoxifen-sensitive MCF7 cells. The model cell lines were treated with the IKK inhibitor parthenolide (PA) or the proteasome inhibitor bortezomib (PS341), alone and in combination with tamoxifen. Expression microarray data available from 54 UCSF node-negative ER-positive breast cancer cases with known clinical outcome were used to search for potential genes signifying upregulated NFκB and AP-1 transcriptional activity in association with tamoxifen resistance. The association of these genes with patient outcome was further evaluated
Overexpression the KCNJ3, a gene that encodes subunit 1 of G-protein activated inwardly rectifying K+ channel (GIRK1) in the primary tumor has been found to be associated with reduced survival times and increased lymph node metastasis in breast cancer patients. In order to survey possible tumorigenic properties of GIRK1 overexpression, a range of malignant mammary epithelial cells, based on the MCF-7 cell line that permanently overexpress different splice variants of the KCNJ3 gene (GIRK1a, GIRK1c, GIRK1d and as a control, eYFP) were produced. Subsequently, selected cardinal neoplasia associated cellular parameters were assessed and compared. Adhesion to fibronectin coated surface as well as cell proliferation remained unaffected. Other vital parameters intimately linked to malignancy, i.e. wound healing, chemoinvasion, cellular velocities / motilities and angiogenesis were massively affected by GIRK1 overexpression. Overexpression of different GIRK1 splice variants exerted differential actions. While
MCF-7 is a breast cancer cell line isolated in 1970 from a 69-year-old Caucasian woman. MCF-7 is the acronym of Michigan Cancer Foundation-7, referring to the institute in Detroit where the cell line was established in 1973 by Herbert Soule and co-workers. The Michigan Cancer Foundation is now known as the Barbara Ann Karmanos Cancer Institute. Prior to MCF-7, it was not possible for cancer researchers to obtain a mammary cell line that was capable of living longer than a few months. The patient, Frances Mallon died in 1970. Her cells were the source of much of current knowledge about breast cancer. At the time of sampling, she was a nun in the convent of Immaculate Heart of Mary in Monroe, Michigan under the name of Sister Catherine Frances. MCF-7 and two other breast cancer cell lines, named T-47D and MDA-MB-231, account for more than two-thirds of all abstracts reporting studies on mentioned breast cancer cell lines, as concluded from a Medline-based survey. MCF-7 cells have the following ...
Foci, nodules of cellular overgrowth, that appear after confluence are an in vitro characteristic of malignant transformation. A well-studied in vitro model of estrogen-dependent tumors is the MCF-7 cell line, derived from a pleural metastasis of a human breast adenocarcinoma. We report that cultivation of MCF-7 cells, using routine methods, results in extensive estrogen-stimulated postconfluent cell accumulation characterized by discrete three-dimensional arrays. Side view Nomarski optical sections revealed these to be principally multicellular foci with occasional domes and pseudoacinar vacuoles. This effect on MCF-7 cell growth occurs in media containing fetal bovine serum but not with calf serum or charcoal-dextran-treated fetal bovine serum unless supplemented with estrogens. Foci formation starts 5-6 days after confluence, and the number of foci generated is a function of the concentration of added estrogens. Foci formation is suppressed by the antiestrogens Tamoxifen and LY 156758. Addition of
Detail záznamu - Neoplastic progression of the human breast cancer cell line G3S1 is associated with elevation of cytoskeletal dynamics and upregulation of MT1-MMP - Detail záznamu - Knihovna Akademie věd České republiky
Study suggests using excess stress to kill therapy resistant breast cancer Maxing out the inherently stressed nature of treatment-resistant breast cancer cells thwarts their adaptive ability to evolve genetic workarounds to treatment, according to a study. Looking at tumor progression as essentially an evolutionary process, researchers highlight the feasibility of maximizing cell stress by inhibiting adaptive pathways to cause cell death ...
MCF-7 and MDA MB 231 cell lines. TSA KRN 633 PDGFR inhibitor and PXD, both the degradation and MG132 dose- Independent Erin sensitive MCF-7 cells, which mediated proteasome to a degradation, but in varying degrees. Ten MCG caused a reduction in low ER, w While TSA and PXD induces a decrease in the ER already 0.5 and 5M, respectively, stabilized by a method MG132. Controlled experiments Showed that the TSA was also the gr Te inhibition of HDAC in both breast cancer cells, such as dose-by-induced increase in acetylated H4 revealed Independent level of histones, w While CG has to be an inhibitor poor or unstable under our experimental its conditions. To modulate the potential of three HDACi-mediated transcription in ER has been studied both in COLLECTING Fig. First The biological activity Th of HDACi on the stability t of various proteins in breast cancer cells. MCF-7 andMDA MB 231cells were exposed or not increasing concentrations of TSA, CG or PXD 20 h in the presence or absence of 5Mof the ...
20(S)-Protopanaxadiol (PPD), a ginsenoside isolated from Pananx quinquefolium L., has been shown to inhibit growth and proliferation in several cancer cell lines. The aim of this study was to evaluate its anticancer activity in human breast cancer cells. MCF-7 cells were incubated with different concentrations of 20(S)-PPD and cytotoxicity was evaluated by MTT assay. Occurrence of apoptosis was detected by DAPI and Annexin V-FITC/PI double staining. Mitochondrial membrane potential was measured with Rhodamine 123. The Bcl-2 and Bax expression were determined by Western blot analysis. Caspase activity was measured by colorimetric assay. 20(S)-PPD dose-dependently inhibited cell proliferation in MCF-7 cells, with an |TEX|$IC_{50}$|/TEX| value of |TEX|$33.3{\mu}M$|/TEX| at 24h. MCF-7 cells treated with 20(S)-PPD presented typical apoptosis, as observed by morphological analysis in cell stained with DAPI. The percentages of annexin V-FITC positive cells were 8.92%, 17.8%, 24.5% and 30.5% in MCF-7 cells
We found that the modified nucleosides 5,6-dihydrouridine (DHU), Ψ, acp3U, 3-methylcytidine (m3C), 5-methyluridine (m5U), 3-methyluridine (m3U), xanthosine (X), 1-methylguanosine (m1G), m22G, N2,N2,7-trimethylguanosine (m2,2,7G), mcm5s2U, N6-threonylcarbamoyladenosine (t6A) and m6t6A are elevated in the supernatants of MCF-7 cells compared to those of MCF-10A cells. Therefore, we generally considered a compound level as "elevated" when the area ratio exceeds the mean value of the reference cell line by two standard deviation values (2σ-concept) [5]. The methylated nucleoside N6-methyladenosine (m6A) is not included in this list because it can be formed through isomerization of 1-methyladenosine (m1A) and thus could not be normalized.. Especially the levels of m5U with ratios ~4/1 (MCF-7/MCF-10A), m2,2,7G (~2:1), m6t6A (~2:1) and acp3U (~2:1) should be pointed out.. m5U is present in eukaryotic tRNA and rRNA [22]. Roe and Tsen postulated, that this nucleoside might be involved in the regulation ...
Gynura procumbens Prevents Chemoresistance through Inhibition MDR1 Expression on MCF-7 Breast Cancer Cell Line and Sensitizes the Cells to Doxorubicin
The growth dependence of many breast cancers on oestrogen has been exploited therapeutically by oestrogen deprivation, but almost all patients eventually develop resistance largely by unknown mechanisms. Wild-type (WT) MCF-7 cells were cultured in oestrogen-deficient medium for 90 weeks in order to …
Protein expression of galectin-7 in breast cancer cell lines.MCF-7 or MDA-MB-231 cells were transfected with an expression vector encoding C/EBPβ-2 before cell
Tspyl2 - mouse gene knockout kit via CRISPR, 1 kit. |dl||dt|Kit Component:|/dt||dd|- |strong|KN318369G1|/strong|, Tspyl2 gRNA vector 1 in |a href=http://www.origene.com/CRISPR-CAS9/Detail.
Nevertheless, if I was diagnosed with early stage luminal breast cancer or DCIS, I would likely opt for intensive therapy, regardless of the risk. I would swallow my concerns and go in, get the surgery, have radiation treatment, if needed anti-hormonal treatment, and perhaps chemo-despite the fact that there is a reasonably high probability that the DCIS or low grade tumor never would have progressed anyway. However, if there was a good biomarker that could be used to determine whether my DCIS would progress or my low grade invasive cancer would metastasize, then I would be empowered to make a more considered decision. Clearly as a clinical community we are over-treating a huge number of individuals, but without good biomarkers and information regarding tumor behavior we are flying half blind. So how do we figure out which ones to treat really aggressively, and which ones not? Those are the kinds of questions we are trying to answer.. Is there an upcoming potential application of your ...
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, ...
Results: Using real-time PCR, to quantify the influence on the expression of the ET axis, we found that ZD4054 significantly reduced ET-1, ETAR, and ECE-1 mRNA expression in MCF-7, MDA-MB-231, and MDA-MB-468 breast cancer cells in a concentration-dependent manner. Furthermore, we investigated the effect of ZD4054 on breast cancer cell proliferation, migration, and invasion. As expected from previous studies, proliferation of breast cancer cells was not affected by ZD4054. However, ZD4054 significantly reduced cellular migration by up to 26.7% (MDA-MB-468; P,0.001) and cellular invasion by up to 46.3% (MCF-7; P,0.001). In aromatase-overexpressing MCF-7aro cells, when either ZD4054 or the aromatase inhibitors were administered alone, there were minimal effects on cellular migration. However, combinations of ZD4054 with either anastrozole or letrozole produced significant reductions in cellular migration (P,0.05). In MCF-7 cells, combination of ZD4054 with the estrogen receptor downregulator, ...
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...
HMGB3 silence inhibits breast cancer cell proliferation and tumor growth by interacting with hypoxia-inducible factor 1alpha Jun Gu, Tao Xu, Qin-Hua Huang, Chu-Miao Zhang, Hai-Yan ChenDepartment of Health Check-Up Center, Jinshan Hospital, Fudan University, Shanghai 201508, Peoples Republic of ChinaBackground: Breast cancer is the most common malignant tumor that affects women with higher incidence. High-mobility group box 3 (HMGB3) plays critical functions in DNA repair, recombination, transcription and replication. This study aimed to investigate the effects of HMGB3 silence on mammosphere formation and tumor growth of breast cancer.Methods: LV5-HMGB3 and LV3-siHMGB3 vectors were transfected into MCF10A, MDA-MB-231, HCC1937, ZR-75-1 and MCF7 cells. Cell counting kit-8 (CCK-8) assay was used to evaluate cell proliferation. Xenograft tumor mice model was established by injection of MDA-MB-231. qRT-PCR and western blot were used to examine the expression of Nanog, Sox2 and OCT-4. Mammosphere forming
HER2 Drives Luminal Breast Cancer Stem Cells in the Absence of HER2 Amplification: Implications for Efficacy of Adjuvant Trastuzumab
BioAssay record AID 103734 submitted by ChEMBL: Compound was tested for cancer cell line growth inhibition against human breast (MCF-7) cell line.
Animated coloured scanning electron micrograph (SEM) of a breast cancer cell growing in culture. It is from the MCF-7 cell line. Magnification: x800 when printed at 10 centimetres wide. - Stock Video Clip K005/6897
miR-126 were over-expressed using the miR-Vec system in highly metastatic LM2 cells. The LM2 cell line are described in detail in Minn et al. Nature 2005 This approach was used to conduct an unbiased search for specific miR-126 target genes in breast cancer cells. 4 Samples
Wnt5a是Wnt家族成员之一[1],其与肿瘤的关系虽有一些研究,但作用尚不清楚[2],有报道认为是促癌基因,也有认为是抑癌基因。同样,Wnt5a在乳腺癌中的作用,特别是与乳腺癌发生发展的重要机制上皮间质转化(epithelial mesenchymal ...