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Transcriptional Analysis of the Effect of Cholinergic Receptor Muscarinic 1 (CHRM1) on Docetaxel Resistance in Human Prostate Cancer Cells

ABSTRACT: Transcriptional Analysis of the Effect of Cholinergic Receptor Muscarinic 1 (CHRM1) on Docetaxel Resistance in Human Prostate Cancer Cells

PROVIDER: PRJNA900260 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22257004_1.fastq.gz	Fastqsanger.gz
	SRR22257004_2.fastq.gz	Fastqsanger.gz
	SRR22257005_1.fastq.gz	Fastqsanger.gz
	SRR22257005_2.fastq.gz	Fastqsanger.gz
	SRR22257006_1.fastq.gz	Fastqsanger.gz

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Cholinergic signaling via muscarinic M1 receptor confers resistance to docetaxel in prostate cancer.

Project description:Docetaxel is the most commonly used chemotherapy for advanced prostate cancer (PC), including castration-resistant disease (CRPC), but the eventual development of docetaxel resistance constitutes a major clinical challenge. Here, we demonstrate activation of the cholinergic muscarinic M1 receptor (CHRM1) in CRPC cells upon acquiring resistance to docetaxel, which is manifested in tumor tissues from PC patients post- vs. pre-docetaxel. Genetic and pharmacological inactivation of CHRM1 restores the efficacy of docetaxel in resistant cells. Mechanistically, CHRM1, via its first and third extracellular loops, interacts with the SEMA domain of cMET and forms a heteroreceptor complex with cMET, stimulating a downstream mitogen-activated protein polykinase program to confer docetaxel resistance. Dicyclomine, a clinically available CHRM1-selective antagonist, reverts resistance and restricts the growth of multiple docetaxel-resistant CRPC cell lines and patient-derived xenografts. Our study reveals a CHRM1-dictated mechanism for docetaxel resistance and identifies a CHRM1-targeted combinatorial strategy for overcoming docetaxel resistance in PC.

| S-EPMC10897519 | biostudies-literature

Transcriptional Analysis of the Effect of Cholinergic Receptor Muscarinic 1 (CHRM1) on Docetaxel Resistance in Human Prostate Cancer Cells

Project description:The overall goal of this study was to investigate the role of CHRM1 in contributing to DTX resistance in human prostate cancer cells.

2023-04-01 | GSE217749 | GEO

Expression data from prostate cancer Docetaxel-resistant cells

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Expression data from Docetaxel-resistant prostate cancer cells

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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Expression data from docetaxel-resistant prostate cancer cell lines

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Expression data from docetaxel-resistant prostate cancer cell lines

Project description:Docetaxel-based chemotherapy is the standard first-line therapy in metastatic castration-resistant prostate cancer. However, most patients eventually develop resistance to this treatment. The aim of the study was to identify key molecular genes and networks associated with docetaxel resistance in 2 models of docetaxel-resistant castration-resistant prostate cancer cell lines. DU-145 and PC-3 cells were converted to docetaxel-resistant cells, DU-145R and PC-3R, respectively. Whole-genome arrays were used to compare global gene expression between these 4 cell lines. Arrays were performed by triplicate for each cell line.

2012-01-01 | E-GEOD-33455 | biostudies-arrayexpress

Prostate cancer cell lines resistant to docetaxel induced by gradient concentration

Project description:We added docetaxel to the culture medium of prostate cancer cell lines PC3 and DU145, and gradually increased the concentration. After a long time of culture, we obtained a docetaxel resistant prostate cancer cell lines.

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Expression data from prostate cancer cell lines C4-2B (docetaxel sensitive) and TaxR (docetaxel resistant) cells

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Expression data from prostate cancer cell lines C4-2B (docetaxel sensitive) and TaxR (docetaxel resistant) cells

Project description:Prostate cancer C4-2B cells were cultured in docetaxel in a dose-escalation manner. After nine months selection, cells were able to divide freely in 5 nM docetaxel, with a specific sets of genes been deregulated. We performed global gene expression analysis by cDNA microarrays to identify genes responsible for docetaxel resistance in TaxR cells. Docetaxel resistant TaxR cells were selected from C4-2B cells during long time docetaxel treatment. Genes responsible for docetaxel resistance were identified using C4-2B vs. TaxR RNA extraction and hybridization on Affymetrix microarrays.

2013-08-01 | E-GEOD-47040 | biostudies-arrayexpress

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

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