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Expression data from breast cancer cell line MCF-7 with ectopic expression of the transcription factor Snail

ABSTRACT: The transcription factor Snail has been proposed to mediate epithelial-to-mesenchymal transition (EMT) and confer mesenchymal invasive phenotype to epithelial cancer cells To analyze the molecular effects of ectopic Snail expression on an epithelial breast cancer cell line, gene expression profiles of MCF-7 cells transfected to overexpress Snail-6SA variant (MCF-7-Snail) and MCF-7 cells transfected with control plasmid (MCF-7-control) were compared. Development of the cell lines has been previously reported by Zhou et al. (PMID: 15448698). Dataset includes 3 replicate cultures of MCF-7-Snail cells and 3 replicate cultures of MCF-7-control cells

ORGANISM(S): Homo sapiens

SUBMITTER: Mezencev Roman

PROVIDER: S-ECPF-GEOD-58252 | biostudies-other |

REPOSITORIES: biostudies-other

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Expression data from breast cancer cell line MCF-7 with ectopic expression of the transcription factor Snail

Project description:The transcription factor Snail has been proposed to mediate epithelial-to-mesenchymal transition (EMT) and confer mesenchymal invasive phenotype to epithelial cancer cells To analyze the molecular effects of ectopic Snail expression on an epithelial breast cancer cell line, gene expression profiles of MCF-7 cells transfected to overexpress Snail-6SA variant (MCF-7-Snail) and MCF-7 cells transfected with control plasmid (MCF-7-control) were compared. Development of the cell lines has been previously reported by Zhou et al. (PMID: 15448698).

2014-07-29 | GSE58252 | GEO

Expression data from breast cancer cell line MCF-7 with ectopic expression of the transcription factor Snail

2014-07-29 | E-GEOD-58252 | biostudies-arrayexpress

Insulin-like growth factor-1 signaling regulates miRNA expression in MCF-7 breast cancer cell line.

Project description:In breast carcinomas, increased levels of insulin-like growth factor 1 (IGF-1) can act as a mitogen to augment tumorigenesis through the regulation of MAPK and AKT signaling pathways. Signaling through these two pathways allows IGF-1 to employ mechanisms that favor proliferation and cellular survival. Here we demonstrate a subset of previously described tumor suppressor and oncogenic microRNAs (miRNAs) that are under the direct regulation of IGF-1 signaling. Additionally, we show that the selective inhibition of either the MAPK or AKT pathways prior to IGF-1 stimulation prevents the expression of previously described tumor suppressor miRNAs that are family and cluster specific. Here we have defined, for the first time, specific miRNAs under the direct regulation of IGF-1 signaling in the estrogen receptor positive MCF-7 breast cancer cell line and demonstrate kinase signaling as a modulator of expression for a small subset of microRNAs. Taken together, these data give new insights into mechanisms governing IGF-1 signaling in breast cancer.

| S-EPMC3511482 | biostudies-literature

Transcription profiling by array of human breast cancer cell line MCF-7 treated with estradiol

Project description:The Estrogen Receptor cofactors SRC1 (NCOA1, KAT13A), SRC2 (NCOA2, GRIP1, TIF2, KAT13C) , SRC3 (NCOA3, AIB1, KAT13B, Rac3) , CBP and p300 are assessed for their genome-wide chromatin binding capacities in the breast cancer cell line MCF7. To determine the Estrogen Receptor dependency of interactions, experiments were performed in the absence of hormone and after Estradiol treatment. In addition, the data were compared with Estrogen Receptor ChIP-seq data from the same timepoint of Estradiol treatment.

| S-ECPF-MTAB-788 | biostudies-other

Cytotoxic properties of titanocenyl amides on breast cancer cell line mcf-7.

Project description:A new titanocenyl amide containing flavone as pendant group has been synthesized by reaction of titanocenyl carboxylic acid chloride and 7-Aminoflavone and structurally characterized by spectroscopic methods. This species and eight previously synthesized titanocenyl amide complexes have been tested in breast adenocarcinoma cancer cell line, MCF-7. The functionalization of titanocene dichloride with amides enhances the cytotoxic activity in MCF-7. Two sets of titanocenyl amides can be identified, with IC(50) <100 muM and IC(50)>100 muM. The most cytotoxic species is Cp(CpCO-NH-C(6)H(4)-(CH(2))(2)CH(3))TiCl(2) with an IC(50) of 24(2) muM, followed by Cp(CpCO-NH-C(6)H(4)-Br)TiCl(2), IC(50) of 46(4) muM and Cp(CpCO-NH-C(6)H(4)-OCF(3))TiCl(2), IC(50) of 49(6) muM. There is no correlation between the nature of the para substituent on the phenyl ring and the cytotoxic properties on MCF-7 cell line.

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The transcription factors Snail and Slug activate the transforming growth factor-beta signaling pathway in breast cancer.

Project description:The transcriptional repressors Snail and Slug are situated at the core of several signaling pathways proposed to mediate epithelial to mesenchymal transition or EMT, which has been implicated in tumor metastasis. EMT involves an alteration from an organized, epithelial cell structure to a mesenchymal, invasive and migratory phenotype. In order to obtain a global view of the impact of Snail and Slug expression, we performed a microarray experiment using the MCF-7 breast cancer cell line, which does not express detectable levels of Snail or Slug. MCF-7 cells were infected with Snail, Slug or control adenovirus, and RNA samples isolated at various time points were analyzed across all transcripts. Our analyses indicated that Snail and Slug regulate many genes in common, but also have distinct sets of gene targets. Gene set enrichment analyses indicated that Snail and Slug directed the transcriptome of MCF-7 cells from a luminal towards a more complex pattern that includes many features of the claudin-low breast cancer signature. Of particular interest, genes involved in the TGF-beta signaling pathway are upregulated, while genes responsible for a differentiated morphology are downregulated following Snail or Slug expression. Further we noticed increased histone acetylation at the promoter region of the transforming growth factor beta-receptor II (TGFBR2) gene following Snail or Slug expression. Inhibition of the TGF-beta signaling pathway using selective small-molecule inhibitors following Snail or Slug addition resulted in decreased cell migration with no impact on the repression of cell junction molecules by Snail and Slug. We propose that there are two regulatory modules embedded within EMT: one that involves repression of cell junction molecules, and the other involving cell migration via TGF-beta and/or other pathways.

| S-EPMC3197668 | biostudies-literature

Snail transcription factor regulates neuroendocrine differentiation in LNCaP prostate cancer cells.

Project description:Snail transcription factor induces epithelial-mesenchymal transition (EMT) via decreased cell adhesion-associated molecules like E-cadherin, and increased mesenchymal markers like vimentin. We previously established Snail-mediated EMT model utilizing androgen-dependent LNCaP cells. These cells express increased vimentin protein and relocalization of E-cadherin from the cell membrane to the cytosol. Interestingly, Snail transfection in LNCaP cells resulted in cells acquiring a neuroendocrine (NE)-like morphology with long neurite-like processes.We tested for expression of NE markers neuron-specific enolase (NSE) and chromogranin A (CgA) by Western blot analysis, and performed proliferation assays to test for paracrine cell proliferation.LNCaP cells transfected with Snail displayed increase in the NE markers, NSE and CgA as well as translocation of androgen receptor (AR) to the nucleus. LNCaP C-33 cells that have been previously published as a neuroendocrine differentiation (NED) model exhibited increased expression levels of Snail protein as compared to LNCaP parental cells. Functionally, conditioned medium from the LNCaP-Snail transfected cells increased proliferation of parental LNCaP and PC-3 cells, which could be abrogated by NSE/CgA siRNA. Additionally, NED in LNCaP-C33 cells or that induced in parental LNCaP cells by serum starvation could be inhibited by knockdown of Snail with siRNA.Overall our data provide evidence that Snail transcription factor may promote tumor aggressiveness in the LNCaP cells through multiple processes; induction of EMT may be required to promote migration, while NED may promote tumor proliferation by a paracrine mechanism. Therefore, therapeutic targeting of Snail may prove beneficial in not only abrogating EMT but also NED.

| S-EPMC2877267 | biostudies-literature

Piezo1 forms mechanosensitive ion channels in the human MCF-7 breast cancer cell line.

Project description:Mechanical interaction between cells - specifically distortion of tensional homeostasis-emerged as an important aspect of breast cancer genesis and progression. We investigated the biophysical characteristics of mechanosensitive ion channels (MSCs) in the malignant MCF-7 breast cancer cell line. MSCs turned out to be the most abundant ion channel species and could be activated by negative pressure at the outer side of the cell membrane in a saturable manner. Assessing single channel conductance (G?) for different monovalent cations revealed an increase in the succession: Li(+) < Na(+) < K(+) ?Rb(+) ? Cs(+). Divalent cations permeated also with the order: Ca(2+) < Ba(2+). Comparison of biophysical properties enabled us to identify MSCs in MCF-7 as ion channels formed by the Piezo1 protein. Using patch clamp technique no functional MSCs were observed in the benign MCF-10A mammary epithelial cell line. Blocking of MSCs by GsMTx-4 resulted in decreased motility of MCF-7, but not of MCF-10A cells, underscoring a possible role of Piezo1 in invasion and metastatic propagation. The role of Piezo1 in biology and progression of breast cancer is further substantiated by markedly reduced overall survival in patients with increased Piezo1 mRNA levels in the primary tumor.

| S-EPMC4322926 | biostudies-literature

Transcription profiling of MCF-7 Human Breast Cancer Cells

Project description:SOX genes encode a family of high-mobility group transcription factors that play critical roles in organogenesis. Virtually all members of SOX family have been found to be deregulated in tumors of various origins. However, little is known about the cellular and molecular behaviours involved in the oncogenic potential of SOX proteins. Cell culture experiments, tissue analysis, and molecular profiling revealed that SOX2 promotes cell proliferation and tumorigenesis through its transcription regulation of cell cycle related genes in breast cancer cells Experiment Overall Design: To delineate the molecular mechanism underlying the cell proliferation and tumorigenic properties of SOX2, we investigated the gene expression profile in MCF-7 cells. Briefly, MCF-7 cells were transfected with pcDNA3.1 and Human SOX2 expression constructs respectively. 24 hours after transfection, total RNA collected from control and SOX2-overexpressing MCF-7 cells was used to probe Human Genome GeneChip array U133 Plus 2.0

| S-ECPF-GEOD-11330 | biostudies-other

Evidence of a genomic biomarker in normal human epithelial mammary cell line, MCF-10A, that is absent in the human breast cancer cell line, MCF-7.

Project description:This study investigated the use of DNA amplification fingerprinting (DAF) to identify biomarkers useful in the elucidating genetic factors that lead to carcinogenesis. The DNA amplification fingerprinting (DAF) technique was used to generate fingerprint profiles of a normal human mammary epithelial cell line (MCF-10A) and a human breast cancer cell line (MCF-7). When compared with one another, a polymorphic biomarker gene (262 base pairs (bps)) was identified in MCF-10A but was not present in MCF-7. This gene was cloned from the genomic DNA of the MCF-10A cell line, and subjected to Genbank database analysis. The analysis of the nucleotide sequence polymorphic marker (Genbank account: AC079630) shows that this biomarker has 100% homology with the nucleotide sequence of human chromosome 12 BAC RP11-476D10 (bps 19612-19353). The nucleotide sequence was used for possible protein translation product and the result obtained indicated that the gene codes for hypothetical protein XF2620. In order to evaluate the effects that the 262 bps biomarker would have on the morphology of MCF-7 cells, it was transfected into MCF-7 cells. There were observable changes in the morphology of the transfected cells. These changes included an increase in cell elongation and a decrease in cell aggregation.

| S-EPMC1510942 | biostudies-literature

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