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A kinome-wide CRISPR screen identifies CK1α as a novel target to overcome enzalutamide resistance of prostate cancer

ABSTRACT: A kinome-wide CRISPR screen identifies CK1α as a novel target to overcome enzalutamide resistance of prostate cancer

PROVIDER: PRJNA839635 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19309802_1.fastq.gz	Fastqsanger.gz
	SRR19309802_2.fastq.gz	Fastqsanger.gz
	SRR19309803_1.fastq.gz	Fastqsanger.gz
	SRR19309803_2.fastq.gz	Fastqsanger.gz
	SRR19309804_1.fastq.gz	Fastqsanger.gz

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A kinome-wide CRISPR screen identifies CK1α as a novel target to overcome enzalutamide resistance of prostate cancer

Project description:Utilizing a kinome-wide CRISPR-Cas9 knockout screen, we identified casein kinase 1 alpha (CK1α) as a novel therapeutic target to overcome enzalutamide resistance. To dissect the underlying mechanisms of targeting CK1α to sensitize cancer cells to ENZA, we performed RNA sequencing of 22Rv1 cells upon CK1α knockout or overexpression. We found that CK1α regulated double-strand break (DSB)-response signaling.

2023-03-10 | GSE203362 | GEO

A kinome-wide CRISPR screen identifies CK1α as a target to overcome enzalutamide resistance of prostate cancer.

Project description:Enzalutamide (ENZA), a second-generation androgen receptor antagonist, has significantly increased progression-free and overall survival of patients with metastatic prostate cancer (PCa). However, resistance remains a prominent obstacle in treatment. Utilizing a kinome-wide CRISPR-Cas9 knockout screen, we identified casein kinase 1α (CK1α) as a therapeutic target to overcome ENZA resistance. Depletion or pharmacologic inhibition of CK1α enhanced ENZA efficacy in ENZA-resistant cells and patient-derived xenografts. Mechanistically, CK1α phosphorylates the serine residue S1270 and modulates the protein abundance of ataxia telangiectasia mutated (ATM), a primary initiator of DNA double-strand break (DSB)-response signaling, which is compromised in ENZA-resistant cells and patients. Inhibition of CK1α stabilizes ATM, resulting in the restoration of DSB signaling, and thus increases ENZA-induced cell death and growth arrest. Our study details a therapeutic approach for ENZA-resistant PCa and characterizes a particular perspective for the function of CK1α in the regulation of DNA-damage response.

| S-EPMC10140619 | biostudies-literature

Genome-wide CRISPR Knockout Screen in LNCaP Cells Treated with Enzalutamide

Project description:To categorize gene loss events in enzalutamide-treated LNCaP cells, a genome-wide CRISPR knockout (KO) screen was performed. We quantified sgRNA abundance between initial and final timepoints in DMSO and enzalutamide treated cell populations

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Targeting DNMTs to overcome enzalutamide resistance in prostate cancer

Project description:Targeting DNMTs to overcome enzalutamide resistance in prostate cancer

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Synthetic lethal siRNA screen for TN-IBC cell line SUM149PT using kinome library with EPA treatment

Project description:Synthetic lethal siRNA screen using a kinome library containing 939 druggable genes in the TN-IBC cell line SUM149PT, in combination with EPA treatment.

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Targeting DNMTs to overcome enzalutamide resistance in prostate cancer

Project description:Prostate cancer is the second leading cause of cancer death among men in the United States. The androgen receptor (AR) antagonist enzalutamide is a FDA-approved drug for treatment of patients with late-stage prostate cancer and is currently under clinical study for early-stage prostate cancer treatment. After a short positive response period to enzalutamide, tumors will develop drug resistance. In this study, we uncovered that DNA methylation was deregulated in enzalutamide-resistant cells. DNMT activity and DNMT3B expression were upregulated in resistant cell lines. Enzalutamide induced the expression of DNMT3A and DNMT3B in prostate cancer cells with a potential role of p53 and pRB in this process. The overexpression of DNMT3B3, a DNMT3B variant, promoted an enzalutamide-resistant phenotype in C4-2B cell lines. Inhibition of DNA methylation and DNMT3B knockdown induced a re-sensitization to enzalutamide. Decitabine treatment in enzalutamide-resistant cells induced a decrease of the expression of AR-V7 and changes of genes for apoptosis, DNA repair and mRNA splicing. Combination treatment of Decitabine and enzalutamide induced a decrease of tumor weight, Ki-67 and AR-V7 expression and an increase of cleaved-caspase3 levels in 22Rv1 xenografts. The collective results suggest that DNA methylation pathway is deregulated after enzalutamide resistance onset and that targeting DNA methyltransferases restores the sensitivity to enzalutamide in prostate cancer cells.

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Genome-wide CRISPR Knockout Screen in LNCaP Cells Treated with Enzalutamide

Project description:Genome-wide CRISPR Knockout Screen in LNCaP Cells Treated with Enzalutamide

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