ATAC-seq to investigate rewiring the transcriptome of castration-resistant prostate cancer through CDK9 inhibition dataset 1

ABSTRACT: The rewiring of transcriptional and epigenetic programs is a hallmark of cancer and a targetable vulnerability for treating metastatic cancers. CDK9, whose primary function is to promote transcriptional elongation at active gene promoters, is emerging as a therapeutic target with broad efficacy in various cancer types. We used the novel and selective CDK9 inhibitor PRT2527 to demonstrate this approach's therapeutic efficacy and tolerability in multiple preclinical tumor models with specific transcriptional dependencies. In castration-resistant prostate cancer (CRPC), PRT2527 inhibited CDK9, AR and other transcription factors (e.g., c-MYC, STAT3, and NF-B) implicated in disease progression and treatment resistance. PRT2527 reduced the proliferation of tumor cell lines and the growth of 3D

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Homo sapiens

SUBMITTER: Giada Sandrini 

PROVIDER: E-MTAB-12986 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress