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Paxillin regulates genomic networks in prostate cancer

ABSTRACT: Paxillin regulates genomic networks in prostate cancer

PROVIDER: PRJNA544533 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9116850_1.fastq.gz	Fastqsanger.gz
	SRR9116850_2.fastq.gz	Fastqsanger.gz
	SRR9117030.fastq.gz	Fastqsanger.gz
	SRR9117120.fastq.gz	Fastqsanger.gz
	SRR9116851_1.fastq.gz	Fastqsanger.gz

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Paxillin regulates genomic networks in prostate cancer [PC3]

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

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Paxillin regulates genomic networks in prostate cancer [LNCaP]

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

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

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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.

2019-08-01 | GSE131730 | GEO

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

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

2019-08-01 | GSE131728 | GEO

Paxillin regulates genomic networks in prostate cancer

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

2019-08-01 | GSE131731 | GEO

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

Integrative miRNA networks predict prostate cancer recurrence

Project description:Integrative miRNA networks predict prostate cancer recurrence

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Endogenous androgen receptor proteomic profiling reveals genomic subcomplex involved in prostate tumorigenesis

Project description:Androgen receptor (AR) is a key player in prostate cancer development and progression. Here we applied immunoprecipitation mass spectrometry of endogenous AR in LNCaP cells to identify components of the AR transcriptional complex. In total, 66 known and novel AR interactors were identified in the presence of synthetic androgen, most of which were critical for AR-driven prostate cancer cell proliferation. A subset of AR interactors required for LNCaP proliferation were profiled using chromatin immunoprecipitation assays followed by sequencing, identifying distinct genomic subcomplexes of AR interaction partners. Interestingly, three major subgroups of genomic subcomplexes were identified, where selective gain of function for AR genomic action in tumorigenesis was found, dictated by FOXA1 and HOXB13. In summary, by combining proteomic and genomic approaches we reveal subclasses of AR transcriptional complexes, differentiating normal AR behavior from the oncogenic state. In this process, the expression of AR interactors has key roles by reprogramming the AR cistrome and interactome in a genomic location-specific manner.

2017-10-27 | PXD008056 | Pride

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