RNA Splicing of the BHC80 Gene Contributes to Neuroendocrine Prostate Cancer Progression

Eur Urol. 2019 Aug;76(2):157-166. doi: 10.1016/j.eururo.2019.03.011. Epub 2019 Mar 23.

Abstract

Background: Prostate adenocarcinoma (AdPC) progression to treatment-induced neuroendocrine prostate cancer (t-NEPC) is associated with poor patient survival. While AdPC and t-NEPC share similar genomes, they possess distinct transcriptomes, suggesting that RNA splicing and epigenetic mechanisms may regulate t-NEPC development.

Objective: To characterize the role of alternative RNA splicing of the histone demethylase BHC80 during t-NEPC progression.

Design, setting, and participants: The expression of BHC80 splice variants (BHC80-1 and BHC80-2) were compared between AdPC and t-NEPC patient tumors. Regulatory mechanisms of RNA splicing of the BHC80 gene were studied, and the signal pathways mediated by BHC80 splice variants were investigated in t-NEPC cell and xenograft models.

Results: Global transcriptome analyses identified that the BHC80-2 variant is highly expressed in t-NEPC. Compared with the known histone demethylation activities of the BHC80 gene, we discovered a novel nonepigenetic action of BHC80-2, whereby BHC80-2 is localized in the cytoplasm to trigger the MyD88-p38-TTP pathway, which results in increased RNA stability of multiple tumor-promoting cytokines. While BHC80-2 does not induce neuroendocrine differentiation of cancer cells, it stimulates cell proliferation and tumor progression independent of androgen receptor signaling. Blockade of BHC80-2-regulated MyD88 signaling suppresses growth of several t-NEPC cell spheroid and xenograft models.

Conclusions: Gain of function of BHC80-2 through alternative RNA splicing activates immune responses of cancer cells to promote t-NEPC development.

Patient summary: The main obstacle to develop effective therapies for patients with t-NEPC is the lack of understanding on how t-NEPC is developed. Our study not only identifies a previously unknown BHC80-2-MyD88 signaling pathway that plays an important role during t-NEPC development, but also provides a proof of principle that targeting this signal pathway may offer an avenue to treat t-NEPC.

Keywords: Alternative RNA splicing; BHC80; SRRM4; Treatment-induced neuroendocrine prostate cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / genetics*
  • Animals
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Disease Progression*
  • Gene Expression Profiling
  • Genetic Variation
  • Histone Deacetylases / genetics*
  • Humans
  • Male
  • Mice
  • Myeloid Differentiation Factor 88 / metabolism
  • Neoplasm Transplantation
  • Nerve Tissue Proteins / genetics
  • Neuroendocrine Tumors / genetics*
  • Neuroendocrine Tumors / metabolism
  • Prostatic Neoplasms / genetics*
  • Protein Isoforms / genetics
  • RNA Splicing*
  • Signal Transduction / genetics
  • Spheroids, Cellular
  • Tristetraprolin / metabolism
  • Tumor Cells, Cultured
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • MYD88 protein, human
  • Myeloid Differentiation Factor 88
  • Nerve Tissue Proteins
  • Protein Isoforms
  • SRRM4 protein, human
  • Tristetraprolin
  • ZFP36 protein, human
  • p38 Mitogen-Activated Protein Kinases
  • PHF21A protein, human
  • Histone Deacetylases