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SETD4 inhibits prostate cancer development by promoting H3K27me3-mediated NUPR1 transcriptional repression and cell

Chong Wang1, Tao Wang2, Kang-Jing Li1

  • 1Department of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.

Cancer Letters
|October 25, 2023
PubMed

Insights

SETD4, a histone methyltransferase, suppresses prostate cancer (PCa) development by regulating H3K27 methylation and the Akt pathway. Its downregulation correlates with poorer PCa prognosis, suggesting therapeutic potential.

Area of Science:

  • Epigenetics
  • Molecular Oncology
  • Biochemistry

Background:

  • Histone lysine methyltransferases, including SETD4, are implicated in various cancers.
  • The specific role of SETD4 in prostate cancer (PCa) pathogenesis is not well understood.
  • SET domain containing 4 (SETD4) functions as a histone methyltransferase.

Purpose of the Study:

  • To investigate the role and mechanism of SETD4 in prostate cancer (PCa).
  • To determine the correlation between SETD4 expression and PCa clinicopathological features.
  • To elucidate the molecular pathways regulated by SETD4 in PCa.

Main Methods:

  • Analysis of SETD4 expression in PCa cell lines and patient tissue samples.
  • SETD4 knockdown experiments to assess effects on cell proliferation and cell cycle.
  • Investigation of SETD4's mechanism involving H3K27 methylation, NUPR1 transcription, and the Akt pathway.

Main Results:

  • SETD4 expression is downregulated in PCa tissues and cells, correlating with inferior clinicopathological characteristics.
  • SETD4 knockdown promotes PCa cell proliferation and accelerates cell cycle progression.
  • SETD4 suppresses NUPR1 transcription via H3K27 methylation (H3K27me3), inactivates the Akt pathway, and impedes PCa tumorigenesis.

Conclusions:

  • SETD4 acts as a tumor suppressor in PCa by catalyzing H3K27 methylation and inhibiting NUPR1 transcription, thereby inactivating the Akt signaling pathway.
  • Decreased SETD4 expression is linked to adverse PCa progression.
  • SETD4 presents a potential target for PCa prognosis and therapeutic strategies.
Keywords:
Histone methyltransferaseProstate cancerSETD4Tumor proliferation

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