The AKR1C3/AR-V7 complex maintains CRPC tumour growth by repressing B4GALT1 expression

Bin Wang, Shiqi Wu, Yong Fang, Guangxi Sun, Dalin He, Jer Tsong Hsieh, Xinyang Wang, Hao Zeng, Kaijie Wu

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


Multiple mechanisms contribute to the survival and growth of metastatic castration-resistant prostate cancer (mCRPC) cells without androgen, including androgen receptor splice variants (AR-V) and de novo intratumoral androgen synthesis. AKR1C3 is a critical androgenic enzyme that plays different roles in mCRPC, such as an EMT driver or AR coactivator. However, the relationship and regulatory mechanisms between AKR1C3 and AR-V remain largely unknown. In this study, we observed a positive correlation between AKR1C3 and AR-V7 staining in tissues from prostate rebiopsy at mCRPC. Mechanistically, AKR1C3 interacts with AR-V7 protein in CRPC cells, which can reciprocally inhibit AR-V7 and AKR1C3 protein degradation. Biologically, this complex is essential for in vitro and in vivo tumour growth of CRPC cells after androgen deprivation as it represses B4GALT1, a unique tumour suppressor gene in PCa. Together, this study reveals AKR1C3/AR-V7 complex as a potential therapeutic target in mCRPC.

Original languageEnglish (US)
Pages (from-to)12032-12043
Number of pages12
JournalJournal of Cellular and Molecular Medicine
Issue number20
StatePublished - Oct 1 2020


  • AKR1C3
  • AR-V7
  • B4GALT1
  • castration-resistant prostate cancer
  • complex

ASJC Scopus subject areas

  • Molecular Medicine
  • Cell Biology


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