Prostate cancer cell lines resistant to docetaxel induced by gradient concentration
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE217452 | GEO | 2022/11/10
REPOSITORIES: GEO
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Project description:Docetaxel is the standard first line therapy for hormone-refractory prostate cancer patients. Here we generated models of Docetaxel resistance in prostate cancer cells to study the molecular pathways that drive the acquisition of resistance to this therapy. We used microarrays to detail the global program of gene expression underlying the acquisition of Docetaxel resistance in prostate cancer cells. Parental Docetaxel-sensitive prostate cancer cell lines (DU145 and 22Rv1) and selected Docetaxel-resistant cells (DU145-DR and 22Rv1-DR) were harvested for RNA extraction and hybridization on Affymetrix microarrays. Samples were analyzed in triplicates in order to increase the resolution of expression profiles.
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Project description:The majority of prostate cancer (PCa) patients treated with docetaxel develop resistance to it. In order to better understand the mechanism behind the acquisition of resistance, we conducted single cell total RNA sequencing (sctotal RNA-seq) of docetaxel sensitive and resistant variants of DU145 and PC3 PCa cell lines. Overall, sensitive and resistant cells clustered separately. However, for both cell lines we identified rare sensitive cells that clustered with the resistant cells indicating resistant cells pre-exist in the sensitive population. Differential gene expression analysis between resistant and sensitive cells revealed 182 differentially expressed genes common to both PCa cell lines. A subset of these genes gave a gene expression profile in the resistant-like sensitive cells similar to the resistant cells. Exploration for functional gene pathways identified 218 common pathways between the two cell lines. Protein ubiquitination was the most differentially regulated pathway and was enriched in the resistant cells. Transcriptional regulator analysis identified potential 321 regulators across both cell lines. One of the top regulators identified was nuclear protein 1 (NUPR1). In contrast to the single cell analysis, bulk analysis of the cells did not reveal NUPR1 as a promising candidate. Knockdown and overexpression of NUPR1 in the PCa cells demonstrated that NUPR1 confers docetaxel resistance in both cell lines. Collectively, these data demonstrate the utility of sctotal RNA-seq to identify regulators of drug resistance. Furthermore, NUPR1 was identified as a mediator of PCa drug resistance, which provides the rationale to explore NUPR1 and its target genes to for reversal of docetaxel resistance.
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