Project description:Transcriptional profiling of human prostate and breast epithelial cells with a time course analysis of EZH2 overexpression of cells at 3, 6, 12, 24, 48, and 72 hrs respectively. Keywords: Genetic modification
Project description:Transcriptional profiling of human prostate and breast epithelial cells comparing control siRNA-treated with EZH2-siRNA treated Keywords: Genetic modification
Project description:Overexpression of EZH2 in estrogen receptor negative (ER-) breast cancer promotes metastasis. EZH2 has been mainly studied as the catalytic component of the Polycomb Repressive Complex 2 (PRC2) that mediates gene repression by trimethylating histone H3 at lysine 27 (H3K27me3). However, how EZH2 drives metastasis despite the low H3K27me3 levels observed in ER- breast cancer is unknown. We have shown that in human invasive carcinomas and distant metastases, cytoplasmic EZH2 phosphorylated at T367 is significantly associated with ER- disease and low H3K27me3 levels. Here, we explore the interactome of EZH2 and of a phosphodeficient mutant EZH2_T367A. We identified novel interactors of EZH2, and identified interactions that are dependent on the phosphorylation and cellular localization of EZH2 that may play a role in EZH2 dependent metastatic progression.
Project description:To determine the altered mRNA expression signatures upon overexpressing EZH2 regulated microRNAs in cancer. To identify EZH2 regulated microRNAs in cancer. Two-condition experiment: Each EZH2 microRNA was overexpressed and compared to a control RNA in BT549 breast cancer cells. In DU145 prostate cancer cell EZH2 was knocked down and comapred to EZH2 scrambled siRNA. Other cell lines were monitored for miRNA expression as they are known to have high endogenous levels of EZH2.
Project description:Comparison of control wild-type and Rb-/- prostate epithelial cell lines under untreated and serum-free conditions Keywords = prostate Keywords = epithelial Keywords: other
Project description:EZH2 is frequently over-expressed in aggressive and metastatic solid tumors, including castration resistant prostate cancer (CRPC). We sought to determine EZH2-dependent gene expression programmes in prostate cancer progression, and found an intriguing functional switch of EZH2 from a repressor to an activator during CRPC development. We used microarrays to detail the global profiling of gene expression that are differentially regulated upon EZH2 depletion in two different prostate cancer cell lines. The androgen-dependent prostate cancer cell line LNCaP and the LNCaP-derived androgen-independent cell line LNCaP-abl (abl) were used for this study, as their transcription profiles strongly resemble that of clinical androgen-dependent and castration resistant prostate tumors, respectively. EZH2 was silenced by specific siRNAs in both cell lines, and total RNA was extracted and hybridized on Affymetrix microarrays.
Project description:EZH2 is frequently over-expressed in aggressive and metastatic solid tumors, including castration resistant prostate cancer (CRPC). We sought to determine EZH2-dependent gene expression programmes in prostate cancer progression, and found an intriguing functional switch of EZH2 from a repressor to an activator during CRPC development. We used microarrays to detail the global profiling of gene expression that are differentially regulated upon EZH2 depletion in two different prostate cancer cell lines.
