Splicing targeting approaches highlight actionable vulnerabilities in advanced prostate cancer [22Rv1]
收藏NIAID Data Ecosystem2026-05-01 收录
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https://www.ncbi.nlm.nih.gov/sra/SRP442919
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To investigate if pharmacological inhibition of splicing could uncover novel actionable vulnerabilities in CRPC, we profiled the genome-wide transcriptional changes elicited in 22Rv1 cells by treatment with three drugs that inhibit the splicing through different molecular targets: i. Pladienolide B, that impairs the activity of SF3B1; ii. Indisulam that promote degradation of the splicing factor RBM39; iii. THZ531 inhibits the cyclin dependent kinases (CDK) 12 and 13. Overall design: Poly-A plus RNA-sequencing of 22Rv1 cells treated with Indisulam (3.3µM, 12hrs), or Pladienolide B (10nM, 6hrs) or THZ531 (200nM, 6hrs) or DMSO as control.
创建时间:
2024-03-07



