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FXR splicing by SF3B3 promotes MYC-driven hepatocarcinogenesis.

Xue Wang1,2, Jiahua Luo1, Lifeng Han3

  • 1School of Pharmaceutical Science and Technology, Tianjin University, Tianjin, China.

Hepatology (Baltimore, Md.)
|September 23, 2025
PubMed
Summary
This summary is machine-generated.

MYC oncogene dysregulation drives liver cancer. SF3B3 regulates Farnesoid X receptor (FXR) splicing, impacting MYC-driven hepatocarcinogenesis and offering potential therapeutic targets for hepatocellular carcinoma (HCC).

Keywords:
MYCbile acidfarnesoid X receptorhepatocellular carcinoma

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Area of Science:

  • Hepatology
  • Oncology
  • Molecular Biology

Background:

  • MYC oncogene dysregulation is a key event in hepatocellular carcinoma (HCC).
  • Farnesoid X receptor (FXR), a bile acid receptor, is a potential therapeutic target for liver diseases.
  • Altered bile acid composition and FXR isoforms are observed in human HCCs.

Purpose of the Study:

  • To investigate the roles of bile acid composition and FXR isoforms in MYC-driven hepatocarcinogenesis.
  • To identify molecular mechanisms linking MYC to FXR dysregulation in HCC.

Main Methods:

  • Induction of HCC in mice using MYC and MCL1 oncogenes.
  • UPLC-MS/MS for bile acid analysis, qPCR and Western blot for gene and protein expression.
  • RNA antisense purification-coupled with mass spectrometry (RAP-MS) to identify splicing factors.

Main Results:

  • MYC-driven HCC mice exhibited elevated bile acid levels and suppressed bile salt export pump (BSEP).
  • SF3B3 was identified as a MYC target and regulator of FXR splicing.
  • SF3B3 and FXR modulation impacted hepatocarcinogenesis; combination therapy showed synergistic effects on HCC cells.

Conclusions:

  • SF3B3 is a critical downstream effector of MYC in hepatocarcinogenesis and regulates FXR splicing.
  • SF3B3 and FXR represent druggable targets in MYC-amplified HCC.