Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PPAR[gamma]2 exerts a tumor suppressive effect in human prostate cancer

ABSTRACT: The nuclear receptor PPAR[gamma] is a master regulator controlling energy metabolism and cell fate in the prostate. One advanced human prostate cancer cell line PC3 was used to examine the effects of restoration of PPAR[gamma]2 action. Restoration of PPAR[gamma]2 action in PC3 cells inhibited cell proliferation and migration. PC3-PPAR[gamma]2 cDNA recombinants showed necrosis in cancer region and lymphocyte infiltration in surrounding stroma by H&E staining. They expressed low microtubules associated protein 1 light chain 3 (LC3), and high mixed lineage kinase domain-like (MLKL), CD4 and CD8 protein expression levels compare to the control by IHC staining. Gain-of-function of PPAR[gamma]2 in PC3 cells resulted in reprogramming of lipid and energy metabolism-associated signaling pathways by microarray analysis. These data are consistent with the idea that PPAR[gamma] action specific to PPAR[gamma]2, exerts a crucial tumor suppressive role on triggering autophagy and necroptosis in human prostate cancer initiation and progression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE108309 | GEO | 2020/12/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

E-GEOD-53470

Project description:Transcription profiling by high throughput sequencing of c-JUN and JUND knockdown prostate cancer PC3 cell lines

2025-01-24 | E-GEOD-53470 | ExpressionAtlas

Inhibition of proliferation and induction of autophagy by atorvastatin in PC3 prostate cancer cells correlate with downregulation of Bcl2 and upregulation of miR-182 and p21 [miRNA expression]

Project description:The epidemiologic association between statin use and decreased risk of advanced prostate cancer suggests that statins may inhibit prostate cancer development and/or progression. Studies were performed to determine the effects of a model statin, atorvastatin (ATO), on the proliferation and differentiation of prostate cancer cells, and to identify possible mechanisms of ATO action. ATO inhibited the in vitro proliferation of both LNCaP and PC3 human prostate cancer cells in dose-dependent fashion. The greater inhibitory activity of ATO in PC3 cells was associated with induction of autophagy in that cell line, as demonstrated by increased expression of LC3-II. miR-182 was consistently upregulated by ATO in PC3 cells, but not in LNCaP cells. ATO upregulation of miR-182 in PC3 cells was p53-independent and was reversed by geranylgeraniol. Transfection of miR-182 inhibitors decreased expression of miR-182 by >98% and attenuated the antiproliferative activity of ATO. miR-182 expression in PC3 cells was also increased in response to stress induced by serum withdrawal, suggesting that miR-182 upregulation can occur due to nutritional stress. Bcl2 and p21 were identified to be potential target genes of miR-182 in PC3 cells. Bcl2 was downregulated and p21 was upregulated in PC3 cells exposed to ATO. These data suggest that miR-182 may be a stress-responsive miRNA that mediates ATO action in prostate cancer cells. Gene and miRNA expression in two prostate cancer cell lines treated with Atorvastatin vs. untreated control.

2013-09-30 | E-GEOD-46375 | biostudies-arrayexpress

Inhibition of proliferation and induction of autophagy by atorvastatin in PC3 prostate cancer cells correlate with downregulation of Bcl2 and upregulation of miR-182 and p21 [Gene expression]

2013-09-30 | E-GEOD-46374 | biostudies-arrayexpress

Inhibition of proliferation and induction of autophagy by atorvastatin in PC3 prostate cancer cells correlate with downregulation of Bcl2 and upregulation of miR-182 and p21 [Gene expression]

2013-09-30 | GSE46374 | GEO

Inhibition of proliferation and induction of autophagy by atorvastatin in PC3 prostate cancer cells correlate with downregulation of Bcl2 and upregulation of miR-182 and p21 [miRNA expression]

2013-09-30 | GSE46375 | GEO

Gene expression changes in primary aortic endothelial cells during expression of dominant negative PPAR gamma (V290M).

Project description:Ligand-mediated activation of the nuclear hormone receptor PPAR gamma lowers blood pressure and improves glucose tolerance in humans. Two naturally occurring mutations (P467L, V290M) in the ligand binding domain of PPAR gamma have been described in humans that lead to severe insulin resistance and hypertension. Experimental evidence suggests that these mutant versions of PPAR gamma act in a dominant negative fashion. To better understand the molecular mechanisms underlying PPAR gamma action in the vasculature, we determined the global gene expression profile in primary aortic endothelial cells in response to endothelial cell specific expression of a dominant negative isoform of PPAR gamma (V290M).

2008-07-23 | GSE11870 | GEO

Gene expression changes in mouse aorta during activation of or interference with PPAR gamma signaling.

Project description:Ligand-mediated activation of the nuclear hormone receptor PPAR gamma lowers blood pressure and improves glucose tolerance in humans. Two naturally occurring mutations (P467L, V290M) in the ligand binding domain of PPAR gamma have been described in humans that lead to severe insulin resistance and hypertension. Experimental evidence suggests that these mutant versions of PPAR gamma act in a dominant negative fashion. To better understand the molecular mechanisms underlying PPAR gamma action in the vasculature, we determined the gene expression patterns in mouse aorta in response to activation or interference with the PPAR gamma signaling pathway. Keywords: time course, dose response

2007-12-12 | GSE8949 | GEO

The effects of HNF1b over-expression in PC3 cells

Project description:Genome-wide association studies (GWAS) and fine-mapping have identified several distinct variants within HNF1B associated with risk of prostate cancer, but its mechanism of action in this context is unknown. To determine the effects of HNF1B in prostate cancer, we over-expressed HNF1B in PC3 cells to identify biological pathways affected by this change, and performed in vitro assays to validate our findings.

2017-08-25 | GSE63134 | GEO

The role of CRISP3 in prostate cancer

Project description:Prostate cancer cells (PC3) were treated with purified human recombinant CRISP3 protein or vehicle control for 4 hours before whole cell protein extraction

2020-07-15 | PXD009609 | JPOST Repository

Expression data from prostate cancer and osteoblast co-cultures

Project description:Dynamic interaction between prostate cancer and the bone microenvironment is a major contributor to metastasis of prostate cancer to bone. In this study we utilized an in-vitro co-culture model of PC3 prostate cancer cells and osteoblasts followed by microarray based gene expression profiling to identify previously unrecognized prostate cancer-bone microenvironment interactions. Factors secreted by PC3 cells resulted in the up-regulation of many genes in osteoblasts associated with bone metabolism and cancer metastasis, including Mmp13, Il-6 and Tgfb2, and down-regulation of Wnt inhibitor Sost. To determine whether altered Sost expression in the bone microenvironment has an effect on prostate cancer metastasis, we co-cultured PC3 cells with Sost knockout (SostKO) osteoblasts and wildtype (WT) osteoblasts and identified several genes differentially regulated between PC3-SostKO osteoblast co-cultures and PC3-WT osteoblast co-cultures. Co-culturing PC3 cells with WT osteoblasts up-regulated cancer-associated long noncoding RNA (lncRNA) MALAT1 in PC3 cells. MALAT1 expression was further enhanced when PC3 cells were co-cultured with SostKO osteoblasts and treatment with recombinant Sost down-regulated MALAT1 expression in these cells. Our results suggest that reduced Sost expression in the tumor microenvironment may promote bone metastasis by up-regulating MALAT1 in prostate cancer.

2015-09-30 | GSE73044 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data