Splicing targeting approaches highlight actionable vulnerabilities in triple negative breast cancer

To investigate if pharmacological inhibition of splicing could uncover novel actionable vulnerabilities in TNBC, we profiled the genome-wide transcriptional changes elicited in MDA-MB-231 cells by treatment with Indisulam, that promote degradation of the splicing, and Pladienolide B, that impairs the activity of SF3B1. Overall design: Poly-A plus RNA-sequencing of MDA-MB-231 cells treated with 10 nM Pladienolide B for 6 hours, Indisulam (3.3µM, 12hrs) or DMSO as control.