Project description:Affymetrix microarray data was generated from MCF7 breast cancer cells treated in vitro with siRNAs against 78 transcription factors and signalling molecules. Gene expresion of 78 functionally important molecules were knocked down in MCF7 breast cancer cells using siRNA. Then the gene expression profiles of these MCF7 cells, along with untreated cells and non-targetting control (SICONTROL) treated cells were analysed using microarrays.
Project description:Affymetrix microarray data was generated from MCF7 breast cancer cells treated in vitro with siRNAs against estrogen receptor alpha (ESR1). Gene expresion of estrogen receptor alpha (ESR1) was knocked down in MCF7 breast cancer cells using siRNA. Then the gene expression profiles of these MCF7 cells, along with non-targetting control treated cells were analysed using Affymetrix Human Genome U133 Plus 2.0 microarrays.
Project description:Affymetrix microarray data was generated from MCF7 breast cancer cells treated in vitro with siRNAs against 78 transcription factors and signalling molecules.
Project description:Affymetrix microarray data were generated from A375 melanoma cells treated in vitro with siRNAs against 45 transcription factors and signalling molecules. 45 functionally important molecules were knocked down in A375 melanoma cells by siRNA. Then the gene expression profiles of these A375 cells, along with untreated cells and sRNA control treated cells were analysed by microarrays.
Project description:Analysis of tumor suppression by cell cycle-related genes which are regulated by SCTR(Secretin receptor) at gene expression level. The hypothesis tested in the present study was that SCTR regulates cell cycle-related genes toward tumor suppression in normal breast cells. Results suggest that normal breast cells have tumor suppressor activity when SCTR was knocked down by siRNA. Total RNA obtained from MCF-10A where SCTR was knocked down by siRNA
Project description:The ets transcription factor ELF5 specifies the differentiation of mammary progenitor cells to establish the milk-secreting lineage. ER- and poor prognosis basal breast cancers arise from this progenitor cell and these cancers express high levels of Elf5. Knockdown of ELF5 expression in basal breast cancer cell lines, or forced expression in luminal breast cancer cell lines, resulted in reduced cell proliferation. Transcript profiling and chromatin immunoprecipitation revealed that the transcriptional activity of ELF5 specified the gene expression patterns that distinguish basal from luminal breast cancer, including suppression of FOXA1, GATA3 and ER, key estrogen-action genes. Tamoxifen treatment of luminal MCF7 cells upregulated Elf5 expression and cells that acquired resistance to Tamoxifen became dependent on ELF5 for proliferation. ELF5 is a regulator of breast cancer cell proliferation, transcriptionally specifies the basal molecular subtype and is utilised by ER+ breast cancer cells to escape proliferative arrest caused by Tamoxifen. Elf5 was knocked down via siRNA in basal HCC1937 cell lines, in triplicate. Elf5 was induced in luminal T47D and MCF7 cell lines via a doxycycline inducible expression vector, in duplicate.
Project description:To investigate the function of SNHG14 in breast cancer, we established MDA-MB-231 cell lines in which this gene has been knocked down by siRNA.
Project description:The second leading cause of cancer death for women in the U.S. is breast cancer. Moreover, a significant number of patients with breast tumors acquire resistance to drugs during therapy. To develop targeted therapeutic strategies to combat drug resistance it is essential to understand the basic molecular mechanisms through which cancer cells control sensitivity to chemotherapeutics. To identify new candidate genes and facilitate the discovery of novel drug resistance pathways, we have generated a resistance profile or ?resistome? of etoposide resistant MCF7 breast cancer cells. Differential expression of over 5000 genes (fold change > 2, P value < 0.05) indicate that several drug resistance mechanisms may be operating in these cells, including up-regulation of ABC transporter genes, down-regulation of the drug target and down-regulation of apoptotic genes. Several transcription factors such as RUNX2, SOX9, ETS1 and SMAD3 were up-regulated in the drug resistant cells. Targeted RUNX2 knockdown in the resistant cells using siRNA increased sensitivity to etoposide and also upregulated expression of pro-apoptotic genes indicating that RUNX2 could be a molecular target against etoposide resistance. Differential miRNA (microRNA) expression was observed among the drug resistant and sensitive cells suggesting that miRNA may also play a role in regulation of drug resistance. Hsa-miR-218, which targets ABCC6, was down-regulated in the drug resistant cell line. Transfection of a miR-218 mimic could down-regulate the expression of the efflux pump ABCC6 by 65% in drug resistant cells suggesting that regulation of miRNA may play an important role in etoposide resistance. long summary Refer to individual Series. This SuperSeries is composed of the following subset Series: GSE28413: Expression profile of etoposide-resistant MCF7 (MCF7VP) cells GSE28414: Expression profile of etoposide-resistant MCF7 (MCF7VP) cells with targeted RUNX2 knockdown
