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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 PC3CR compared with PC3.

ORGANISM(S): Homo sapiens

PROVIDER: GSE182619 | GEO | 2021/08/24

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 DU145CR compared with DU145.

2018-08-01 | GSE110107 | GEO

Overcoming ABCB1 mediated multidrug resistance in castration resistant prostate cancer

Project description:The few available therapies for mCRPC patients include taxanes docetaxel (DTX) and cabazitaxel (CBZ). However, development of resistance limits their clinical use. PCa that relapses after hormonal therapies, referred to as castration resistant prostate cancer (CRPC), often presents with metastases (mCRPC) that are the major cause of mortality. The few available therapies for mCRPC patients include taxanes docetaxel (DTX) and cabazitaxel (CBZ). However, development of resistance limits their clinical use. To study taxanes resistance, we produced CBZ resistant C4-2B cells (RC4-2B) and documented resistance to both CBZ and DTX in cell culture and in 3D prostaspheres settings. RNAseq identified increased expression of ABCB1 in RC4-2B, that was confirmed by immunoblotting and immunofluorescent analysis. ABCB1-specific inhibitor elacridar reversed CBZ and DTX resistance in RC4-2B cells, confirming ABCB1-mediated resistance mechanism.

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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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Expression data from docetaxel-resistant and cabazitaxel-resistant prostate cancer cell lines

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.

2020-10-25 | GSE158494 | GEO

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

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

| PRJNA757016 | ENA

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

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

| PRJNA433108 | ENA

RNA-seq Analysis of Castration-Resistant Prostate Cancer With Knock-down of E2F1

Project description:From castration resistant prostate cancer (CRPC) regulatory network, we found over 90% negative feedback loop went through E2F1. And we detected PC3 and DU145 cells with depletion of E2F1 through the invasion, migration, proliferation and apoptosis experiments. In order to identify which genes trigger these phenomenon and regulatory mechanism of E2F1 in CRPC, we performed the gene expression between the vector and under the knockdown of E2F1 in PC3 and DU145 cells by RNA sequencing (RNA-seq). To investigate differentially expressed genes (false discovery rate (FDR) <0.05, |log2 (Fold Change)| > 1) between vector control and shE2F1 of CRPC cells, we performed processing RNA-Seq data using the Basespace. Then we verified some common two cells’ differentially expressed genes through quantitative real-time PCR.

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miR-130a activates apoptotic signaling through activation of caspase-8 in taxane-resistant prostate cancer cells [miRNA]

Project description:Background: The acquisition of drug resistance is one of the most malignant phenotypes of cancer. MicroRNAs (miRNAs) have been implicated in various types of cancers, but its role in taxane-resistance of prostate cancer remains poorly understood. Methods: In order to identify miRNAs related to taxane-resistance, miRNA profiling was performed using prostate cancer PC3 cells and paclitaxel-resistant PC3 cell lines established from PC3 cells. Microarray analysis of mRNA expression was also conducted to search for potential target genes of miRNA. The effects of ectopic expression of miRNA on cell growth, tubulin polymerization, drug sensitivity and apoptotic signaling pathway were investigated in a paclitaxel-resistant PC3 cell line. Results: The expression of miR-130a was down-regulated in all paclitaxel-resistant cell lines compared with parental PC3 cells. Based on mRNA microarray analysis, we identified SLAIN1 and CAV2 as potential target genes for miR-130a. Transfection with a miR-130a precursor into a paclitaxel-resistant cell line suppressed cell growth and increased the sensitivity to paclitaxel. Lastly, ectopic expression of miR-130a did not affect the polymerized tubulin level, but activated apoptotic signaling through activation of caspase-8. Conclusion: These results suggested that miR-130a may be involved in the paclitaxel-resistance and could be a therapeutic target for taxane-resistant prostate cancer.

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miR-130a activates apoptotic signaling through activation of caspase-8 in taxane-resistant prostate cancer cells [total RNA]

2015-07-31 | GSE64012 | GEO

miR-130a activates apoptotic signaling through activation of caspase-8 in taxane-resistant prostate cancer cells [miRNA]

2015-07-31 | E-GEOD-64013 | biostudies-arrayexpress