Chromatin profiles classify castration-resistant prostate cancers suggesting therapeutic targets

Science. 2022 May 27;376(6596):eabe1505. doi: 10.1126/science.abe1505. Epub 2022 May 27.

Abstract

In castration-resistant prostate cancer (CRPC), the loss of androgen receptor (AR) dependence leads to clinically aggressive tumors with few therapeutic options. We used ATAC-seq (assay for transposase-accessible chromatin sequencing), RNA-seq, and DNA sequencing to investigate 22 organoids, six patient-derived xenografts, and 12 cell lines. We identified the well-characterized AR-dependent and neuroendocrine subtypes, as well as two AR-negative/low groups: a Wnt-dependent subtype, and a stem cell-like (SCL) subtype driven by activator protein-1 (AP-1) transcription factors. We used transcriptomic signatures to classify 366 patients, which showed that SCL is the second most common subtype of CRPC after AR-dependent. Our data suggest that AP-1 interacts with the YAP/TAZ and TEAD proteins to maintain subtype-specific chromatin accessibility and transcriptomic landscapes in this group. Together, this molecular classification reveals drug targets and can potentially guide therapeutic decisions.

MeSH terms

  • Cell Line, Tumor
  • Chromatin* / genetics
  • Gene Expression Profiling
  • Humans
  • Male
  • Molecular Targeted Therapy*
  • Neoplastic Stem Cells / classification
  • Neoplastic Stem Cells / metabolism
  • Organoids / metabolism
  • Organoids / pathology
  • Prostatic Neoplasms, Castration-Resistant* / classification
  • Prostatic Neoplasms, Castration-Resistant* / drug therapy
  • Prostatic Neoplasms, Castration-Resistant* / genetics
  • Receptors, Androgen / genetics
  • Receptors, Androgen / metabolism
  • Transcription Factor AP-1 / genetics
  • Transcription Factor AP-1 / metabolism

Substances

  • Chromatin
  • Receptors, Androgen
  • Transcription Factor AP-1