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Genome-wide occupancy of FLAG-MED25 and ETV4 and expression profiling of shRNA-mediated knockdown of ETV4 and MED25 in the prostate cell line PC3

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE133448 | GEO | 2019/06/28

REPOSITORIES: GEO

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shRNA-mediated knockdown of ETV4 and MED25 in the prostate cell line PC3 reveals set of genes potentially coregulated by MED25 and ETV4

Project description:Our in vitro binding studies support a model whereby MED25 exhibits multivalent interactions with a subset of related ETS factors, ETV1/4/5. We hypothesize that the interaction would allow for coregulation of genes by ETV1/4/5 and MED25, acting perhaps to link the ETVs to the Mediator complex. To explore this possibility, we compared the genome occupancy for FLAG-tagged MED25 and ETV4 in the prostate cancer cell line PC3, which overexpresses ETV4. We also tested for relevance of MED25 and ETV4 binding to for gene expression in PC3s. We found a high degree of overlap in the FLAG-MED25 and ETV4 ChIPs datasets consistent with our model, and also identified a subset of target genes co-dependent on Med25 and ETV4.

2019-06-28 | GSE133447 | GEO

Genome-wide occupancy of FLAG-MED25 and ETV4 in PC3 cells

2019-06-28 | GSE133445 | GEO

Genome-wide occupancy of FLAG-MED25 and ETV4 and expression profiling of shRNA-mediated knockdown of ETV4 and MED25 in the prostate cell line PC3

Project description:Genome-wide occupancy of FLAG-MED25 and ETV4 and expression profiling of shRNA-mediated knockdown of ETV4 and MED25 in the prostate cell line PC3

| PRJNA551467 | ENA

Genome-wide occupancy of FLAG-MED25 and ETV4 in PC3 cells

Project description:Genome-wide occupancy of FLAG-MED25 and ETV4 in PC3 cells

| PRJNA551468 | ENA

shRNA-mediated knockdown of ETV4 and MED25 in the prostate cell line PC3 reveals set of genes potentially coregulated by MED25 and ETV4

Project description:shRNA-mediated knockdown of ETV4 and MED25 in the prostate cell line PC3 reveals set of genes potentially coregulated by MED25 and ETV4

| PRJNA551469 | ENA

Gene expression profiles induced by shRNA-mediated knockdown of PDEF in MCF7 mammary epithelial cell line

Project description:Microarray gene expression analysis was performed in MCF7 cells transduced with a non-specific shRNA or PDEF-targeting shRNA, and both subjected to hormone depletion for 48 hours. Analyses of differentially expressed genes combined with gene ontology revealed a downregulation of cell cycle related-genes and an upregulation of apoptosis-related genes in PDEF knockdown cells. These target genes constitute potential effectors of the pro-survival role of PDEF. Four samples were harvested after lentiviral infection with either non-specific shRNA control or PDEF-targetting shRNA. All samples were subjected to hormone depletion for 48 hours. Each condition was performed in duplicate

| S-ECPF-GEOD-40985 | biostudies-other

The ETS gene ETV4 is required for anchorage-independent growth and a cell proliferation gene expression program in PC3 prostate cells.

Project description:Chromosomal abnormalities that give rise to elevated expression levels of the ETS genes ETV1, ETV4, ETV5, or ERG are prevalent in prostate cancer, but the function of these transcription factors in carcinogenesis is not clear. Previous work in cell lines implicates ERG, ETV1, and ETV5 as regulators of invasive growth but not transformation. Here we show that the PC3 prostate cancer cell line provides a model system to study the over-expression of ETV4. Migration assays, anchorage independent growth assays, and microarray analysis indicate that high ETV4 expression contributes to both transformation and cellular motility in PC3 cells. ETV4 directly bound the 5' and 3' MYC enhancers and modulated expression of both MYC and other cell proliferation genes, demonstrating a potential role in cell growth control. Despite this novel role for ETV4 in anchorage independent growth, ETV4 over-expression in normal prostate-derived RWPE-1 cells showed effects similar to ETV1 over-expression - increased cellular motility, and an up-regulation of genes encoding extracellular proteins as well as ones important for development, inflammation, and wound healing. Because ETV1 and ETV4 have similar roles when introduced to the same cellular background, we suggest that the requirement of high ETV4 expression for maintenance of the anchorage-independent growth in PC3 cells is due to a specific characteristic of this cell line rather than a function of ETV4 that is distinct from the other oncogenic ETS genes. Thus, the function of ETS genes in prostate cancer may differ based on other genetic alterations in a tumor.

| S-EPMC3046414 | biostudies-literature

MELK and UBE2C gene knockdown in prostate cancer cell line PC3

Project description:In order to address the putative role of MELK and UBE2C in prostate cancer development and progression, we performed functional analysis upon siRNA-based knockdown, and searched for downstream genes and processes by microarray experiments. RNAi-based inhibition of MELK and UBE2C was efficient in PC3 prostate cancer cells and decreased transcriptional level down to about 30% remaining expression level.

2012-10-19 | GSE32873 | GEO

Effects of Long-Term Citrate Treatment in the PC3 Prostate Cancer Cell Line.

Project description:Acute administration of a high level of extracellular citrate displays an anti-proliferative effect on both in vitro and in vivo models. However, the long-term effect of citrate treatment has not been investigated yet. Here, we address this question in PC3 cells, a prostate-cancer-derived cell line. Acute administration of high levels of extracellular citrate impaired cell adhesion and inhibited the proliferation of PC3 cells, but surviving cells adapted to grow in the chronic presence of 20 mM citrate. Citrate-resistant PC3 cells are significantly less glycolytic than control cells. Moreover, they overexpress short-form, citrate-insensitive phosphofructokinase 1 (PFK1) together with full-length PFK1. In addition, they show traits of mesenchymal-epithelial transition: an increase in E-cadherin and a decrease in vimentin. In comparison with PC3 cells, citrate-resistant cells display morphological changes that involve both microtubule and microfilament organization. This was accompanied by changes in homeostasis and the organization of intracellular organelles. Thus, the mitochondrial network appears fragmented, the Golgi complex is scattered, and the lysosomal compartment is enlarged. Interestingly, citrate-resistant cells produce less total ROS but accumulate more mitochondrial ROS than control cells. Consistently, in citrate-resistant cells, the autophagic pathway is upregulated, possibly sustaining their survival. In conclusion, chronic administration of citrate might select resistant cells, which could jeopardize the benefits of citrate anticancer treatment.

| S-EPMC6600328 | biostudies-literature

MELK and UBE2C gene knockdown in prostate cancer cell line PC3

2012-10-19 | E-GEOD-32873 | biostudies-arrayexpress