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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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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.

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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

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Identification of Genes Promoting Resistance to Enzalutamide

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