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SiRNA profiling of human cancer cell line MDA-MB-231 knocked down for CD146 mRNA

ABSTRACT: Metastasis is a complex process involving loss of adhesion, migration, invasion and proliferation of cancer cells. Cell adhesion molecules play a pivotal role in this phenomenon by regulating cell-cell and cell-matrix interactions. CD146 (MCAM) is associated with advanced tumor stage in melanoma, prostate and ovarian cancers. For this study, the MDA-MB-231 cell line was used as a prototypic mesenchymal and invasive cell line, spontaneously expressing high levels of CD146. Using whole-genome DNA microarrays, we investigated genes for which expression was modified by CD146 down-regulation, obtained by siRNA or shRNA technology Experiment Overall Design: Expression profiles of two cell lines transfected by two differents ShRNA directed against CD146 were compared with expression profiles of 3 control cell lines (i.e. native cell line, empty plasmid and shRNA directed against GFP)

ORGANISM(S): Homo sapiens

SUBMITTER: FINETTI Pascal

PROVIDER: S-ECPF-GEOD-11951 | biostudies-other |

REPOSITORIES: biostudies-other

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siRNA profiling of human cancer cell line MDA-MB-231 knocked down for CD146 mRNA

Project description:Metastasis is a complex process involving loss of adhesion, migration, invasion and proliferation of cancer cells. Cell adhesion molecules play a pivotal role in this phenomenon by regulating cell-cell and cell-matrix interactions. CD146 (MCAM) is associated with advanced tumor stage in melanoma, prostate and ovarian cancers. For this study, the MDA-MB-231 cell line was used as a prototypic mesenchymal and invasive cell line, spontaneously expressing high levels of CD146. Using whole-genome DNA microarrays, we investigated genes for which expression was modified by CD146 down-regulation, obtained by siRNA or shRNA technology Experiment Overall Design: Expression profiles of two cell lines transfected by two differents ShRNA directed against CD146 were compared with expression profiles of 3 control cell lines (i.e. native cell line, empty plasmid and shRNA directed against GFP)

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RNAi profiling of human MDA-MB-231 cells knocked down for RhoGDIbeta

Project description:RhoGDIbeta (ARHGDIB) is often expressed in tumor cells. It negatively regulates Rho-GTPases, but may have other functions as well. To analyze its effect on gene expression, RhoGDIbeta was suppressed by RNA interference in MDA-MB-231 breast cancer cells and changes in gene expression monitored by cDNA microarrays. Experiment Overall Design: MDA-MB-231 cells were either transfected with a RhoGDIbeta-specific siRNA or a control siRNA (siLuc), grown for three days, harvested and lysed for total RNA isolation. RNA was subjected to cDNA microarray analysis by using Affymetrix chip HG-U133A. A total of three independent transfection experiments were performed. The samples obtained from experiments 1, 2 and 3 were designated as siLuc_rep1, siLuc_rep2, siLuc_rep3 (siLuc transfected) and siARH_rep1, siARH_rep2, siARH_rep3 (siRhoGDIbeta transfected), respectively.

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Expression data from ELK3 knocked down MDA-MB-231 cell line.

Project description:Triple-negative breast cancer is a highly aggressive tumor subtype that lacks effective therapeutic targets. Here, we show that ELK3 is overexpressed in a subset of breast cancers, in particular basal-like and normal-like/claudin-low cell lines. Suppression of ELK3 in MDA-MB-231 cells led to transdifferentiation from an invasive mesenchymal phenotype to a non-invasive epithelial phenotype both in vitro and in vivo. Suppression of ELK3 results in the extensive changes in genome expression profiles. Among these, GATA3, a master suppressor of metastasis, was epigenetically activated and we found that suppression of GATA3 led to the restoration of migration and invasion. These results suggest that the ELK3-GATA3 axis is a major pathway that promotes metastasis of MDA-MB-231 cells.

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Expression data from ELK3 knocked down MDA-MB-231 cell line.

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Effects of FSTL1 on cell proliferation in breast cancer cell line MDA‑MB‑231 and its brain metastatic variant MDA‑MB‑231‑BR.

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Transcription profiling by array of MDA-MB-231 cells with HMGA2 knock-down

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Long noncoding RNA and mRNA profiling in MDA-MB-231 cells following RNAi-mediated knockdown of SIRT7.

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RNAi profiling of human MDA-MB-231 cells knocked down for RhoGDIbeta

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