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Analysis of cabazitaxel-resistant mechanism in human castration-resistant prostate cancer

ABSTRACT: To investigate cabazitaxel (CBZ) resistance in prostate cancer, we examined the changes in global gene expression before and after development of acquired CBZ resistance. Functional annotation clustering (FAC) analysis of DAVID showed cell division (GO: 0051301) and mitotic nuclear division (GO: 0007067) were the most enhanced clusters in DU145CR compared with DU145.

ORGANISM(S): Homo sapiens

PROVIDER: GSE110107 | GEO | 2018/08/01

REPOSITORIES: GEO

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Analysis of cabazitaxel-resistant mechanism in human castration-resistant prostate cancer

Project description:To investigate cabazitaxel (CBZ) resistance in prostate cancer, we examined the changes in global gene expression before and after development of acquired CBZ resistance. Functional annotation clustering (FAC) analysis of DAVID showed cell division (GO: 0051301) and mitotic nuclear division (GO: 0007067) were the most enhanced clusters in PC3CR compared with PC3.

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Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. Although initially hormone-deprovation therapy is effective to inhibit cancer progression, most of cancers relapse as castration-resistant prostate cancer (CRPC). In this study, we examined the effect of OCT4 or NRF1 knockdown in CRPC cells. In order to investigate the OCT4 and NRF1 function in CRPC cells, we performed gene expression in AR-positive CRPC cell line, 22Rv1, AR-negative CRPC cell lines, PC3-CR (Cabazitaxel resistant), DU145, and DU145-CR, after siOCT4 (10 nM) or siNRF1 (10 nM) treatment. We also treated cells with vehicle, ribavirin (riba), or dihydrotestosterone (DHT) to analyzed the effects of thiese drug treatments.

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Project description:Docetaxel and cabazitaxel are the chemotherapy agents used in castration-resistant prostate cancer. However, most patients eventually develop resistance to these treatments. The aim of the study was to identify key molecular genes and networks associated with taxanes resistance in 2 models of docetaxel-resistant and cabazitaxel-resistant castration-resistant prostate cancer cell lines.

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Project description:We performed RNA-seq and ChIP-seq in three prostate cell lines (VCaP, LNCaP and DU145) to ascertain the role of the mediator complex MED1 in AR signaling. Upon androgen stimulation, MED1 undergoes phosphorylation by CDK7 and physically engages with AR at super-enhancer sites, which is essential for AR-mediated transcription. The CDK7 specific inhibitor THZ1 blunts AR-dependent neoplastic growth by preventing the co-recruitment of AR/MED1 in a genome-wide fashion, and reverts the enzalutamide resistance characterized by hyper-phosphorylated MED1. The effect of THZ1 phenocopies that for MED1 and CDK7 knockdown.

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Analysis of cabazitaxel-resistant mechanism in human castration-resistant prostate cancer

Project description:Analysis of cabazitaxel-resistant mechanism in human castration-resistant prostate cancer

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Analysis of cabazitaxel-resistant mechanism in human castration-resistant prostate cancer

Project description:Analysis of cabazitaxel-resistant mechanism in human castration-resistant prostate cancer

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ATF6 is required for the survival of castration-resistant prostate cancer cells

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