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FXR induces SOCS3 and suppresses hepatocellular carcinoma

Fei Guo1, Zhizhen Xu2, Yan Zhang2

  • 1Department of Hepatobiliary Surgery Institute, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.

Oncotarget
|September 30, 2015
PubMed

Insights

Farnesoid X Receptor (FXR) activation inhibits liver cancer growth by increasing Suppressor of cytokine signaling 3 (SOCS3). This FXR-SOCS3 pathway offers a new target for hepatocellular carcinoma (HCC) prevention and treatment.

Area of Science:

  • Hepatology
  • Molecular Biology
  • Oncology

Background:

  • Suppressor of cytokine signaling 3 (SOCS3) inhibits liver carcinogenesis via STAT3 signaling.
  • Farnesoid X Receptor (FXR) protects against hepatocellular carcinoma (HCC).

Purpose of the Study:

  • To investigate if FXR's tumor-suppressive activity involves SOCS3 regulation.
  • To elucidate the molecular mechanism of FXR in HCC.

Main Methods:

  • FXR activation using GW4064 in HCC cells.
  • SOCS3 knockdown via siRNA.
  • Reporter assays, EMSA, and ChIP assays.
  • In vivo HCC xenograft studies in nude mice.

Main Results:

  • FXR activation inhibited HCC cell growth, induced G1 cell cycle arrest, and repressed STAT3 activity.
  • FXR enhanced SOCS3 promoter activity, directly binding to its promoter region.
  • FXR activation up-regulated SOCS3 and p21 expression, inhibiting STAT3 phosphorylation in vivo.

Conclusions:

  • FXR exerts anti-HCC effects through SOCS3 induction.
  • The FXR-SOCS3 signaling pathway is a potential therapeutic target for HCC.
Keywords:
FXRHCCSOCS3STAT3

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