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Paxillin regulates genomic networks in prostate cancer [C4-2]

ABSTRACT: We report that the adaptor protein, paxillin, regulates some androgen responsive genes in the castration resistant prostate cancer cell line,C4-2.

ORGANISM(S): Homo sapiens

PROVIDER: GSE131728 | GEO | 2019/08/01

REPOSITORIES: GEO

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Paxillin regulates genomic networks in prostate cancer [LNCaP]

Project description:We report that the adaptor protein, paxillin, regulates some androgen responsive genes in the castration sensitive prostate cancer cell line, LNCaP.

2019-08-01 | GSE131726 | GEO

Paxillin regulates genomic networks in prostate cancer [PC3]

Project description:We report that the adaptor protein, paxillin, regulates some proliferative and apoptotic genes in the castration resistant prostate cancer cell line, PC3.

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Paxillin regulates genomic networks in prostate cancer [C4-2]

Project description:Paxillin regulates genomic networks in prostate cancer [C4-2]

| PRJNA544528 | ENA

Paxillin regulates genomic networks in prostate cancer

Project description:Paxillin regulates genomic networks in prostate cancer

| PRJNA544533 | ENA

Paxillin regulates genomic networks in prostate cancer [PC3]

Project description:Paxillin regulates genomic networks in prostate cancer [PC3]

| PRJNA544534 | ENA

Paxillin regulates genomic networks in prostate cancer [LNCaP]

Project description:Paxillin regulates genomic networks in prostate cancer [LNCaP]

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Gene Expression in Castration-Resistant C4-2 Cells after AR Knockdown

Project description:Prostate cancer is the most common, lethal malignancy in men. Although androgen withdrawal therapies are used to treat advanced disease, progression to a castration-resistant, end-stage is the usual outcome. In this study, the tested hypothesis was that the androgen receptor remains essential for the growth and viability of castration-resistant disease. Knocking down the androgen receptor in well-established tumors grown in castrated mice caused growth arrest, decreased serum PSA, and frequently regression and total eradication of tumors. Growth control of castration-resistant tumors appeared to be linked to the extent of androgen receptor knockdown, which triggers upregulation of many genes involved in apoptosis, cell cycle arrest, and inhibition of tumorigenesis and protein synthesis. Our findings provide proof of principle that in vivo knockdown of the androgen receptor is a viable therapeutic strategy to control and possibly eradicate prostate cancers that have progressed to the lethal castration-resistant state. C4-2 human prostate cancer cells stably expressing a tetracycline-inducible AR-targeted short hairpin RNA (shRNA) or scrambled shRNA were generated. These two cell lines were incubated in the absence of androgens with or without doxycycline hyclase (DOX). Comparison analysis of the gene expression profiles of C4-2 cells stably expressing AR shRNA + DOX and control cells (AR shRNA - DOX and scrambled shRNA Â± DOX) was conducted to identify differentially regulated genes due to AR knockdown after normalization and data filtering. Genes were considered to be significantly different if the expression in the induced AR shRNA + DOX cells was at least 1.7-fold greater or 1.7-fold less than that seen in the control cells, with P< 0.05.

2010-06-23 | E-GEOD-13332 | biostudies-arrayexpress

Paxillin regulated genomic networks in prostate cancer.

Project description:Paxillin is extensively involved in focal adhesion signaling and kinase signaling throughout the plasma membrane and cytoplasm. However, recent studies in prostate cancer suggest that paxillin also plays a critical role in regulating gene expression within the nucleus, serving as a liaison between cytoplasmic and nuclear MAPK and Androgen Receptor (AR) signaling. Here we used RNA-seq to examine the paxillin-regulated transcriptome in several human prostate cancer cell lines. First, we examined paxillin effects on androgen-mediated transcription in control or paxillin-depleted AR-positive LNCaP and C4-2 human prostate cancer cells. In androgen-dependent LNCaP cells, we found over 1000 paxillin-dependent androgen-responsive genes, some of which are involved in endocrine therapy resistance. Most paxillin-dependent AR-mediated genes in LNCaP cells were no longer paxillin-dependent in androgen-sensitive, castration-resistant C4-2 cells, suggesting that castration-resistance may markedly alter paxillin effects on genomic AR signaling. To examine the paxillin-regulated transcriptome in the absence of androgen signaling, we performed RNA-seq in AR-negative PC3 human prostate cancer cells. Paxillin enhanced several pro-proliferative pathways, including the CyclinD/Rb/E2F and DNA replication/repair pathways. Additionally, paxillin suppressed pro-apoptotic genes, including CASP1 and TNFSF10. Quantitative PCR confirmed that these pathways are similarly regulated by paxillin in LNCaP and C4-2 cells. Functional studies showed that, while paxillin stimulated cell proliferation, it had minimum effect on apoptosis. Thus, paxillin appears to be an important transcriptional regulator in prostate cancer, and analysis of its transcriptome might lead to novel approaches toward the diagnosis and treatment of this important disease.

| S-EPMC6802295 | biostudies-literature

Paxillin regulates genomic networks in prostate cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-08-01 | GSE131731 | GEO

Comparison of the prostate cancer cell line LNCaP and its androgen insensitive derivative C4-2B

Project description:LNCaP and its androgen insensitive derivative were profiled in order to identify genes differentially expressed during the conversion to androgen insensitivity. This experiment was performed due to the presence of an ins(7;14) localizing the entire ETV1 locus to chr 14 in LNCaP and C4-2B prostate cancer cells. Keywords: cell type comparison LNCaP and C4-2B were both hybridized to Agilent Whole Human Genome Oligonucleotide Microarrays, with a commercially obtained pool of benign prostate RNA serving as the reference for both cell lines. Dye flips for both cell lines were also performed

2007-08-07 | E-GEOD-7702 | biostudies-arrayexpress

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