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FXR blocks the growth of liver cancer cells through inhibiting mTOR-s6K pathway

Xiongfei Huang1, Yeting Zeng2, Xinrui Wang3

  • 1Department of Pathology and Institute of Oncology, Preclinical School, Fujian Medical University, Fuzhou 350108, Fujian, China; Key Laboratory of Ministry of Education for Gastrointestinal Cancer, Fujian Medical University, Fuzhou 350108, Fujian, China.

Biochemical and Biophysical Research Communications
|April 26, 2016
PubMed

Insights

Farnesoid X Receptor (FXR) acts as a liver cancer tumor suppressor by inhibiting the mTOR/S6K pathway. FXR levels can guide personalized treatment with mTOR inhibitors for liver cancer patients.

Area of Science:

  • Hepatology
  • Molecular Oncology
  • Cancer Biology

Background:

  • The nuclear receptor Farnesoid X Receptor (FXR) is implicated as a tumor suppressor in liver tissue.
  • The precise molecular mechanisms underlying FXR's tumor-suppressive functions in hepatocellular carcinoma remain incompletely elucidated.

Purpose of the Study:

  • To investigate the role of FXR in regulating signaling pathways involved in liver cancer cell proliferation.
  • To explore the potential of FXR as a biomarker for predicting response to mTOR-targeted therapies in liver cancer.

Main Methods:

  • Gene expression profiling of human liver cancer cells using microarrays.
  • Bioinformatics analysis to identify potential FXR-regulated pathways.
  • Experimental manipulation of FXR expression levels in vitro and in vivo models.
  • Assessment of cell proliferation, cell cycle arrest, and signaling pathway activation (mTOR/S6K).

Main Results:

  • Bioinformatics analysis suggested FXR regulates the mTOR/S6K signaling pathway.
  • Overexpression of FXR inhibited liver cancer cell growth and induced cell cycle arrest, an effect potentiated by rapamycin (an mTOR/S6K inhibitor).
  • FXR downregulation promoted cell growth, while FXR upregulation enhanced rapamycin's inhibitory effects. Ectopic FXR expression in xenografts suppressed tumor growth and reduced p-S6K levels.

Conclusions:

  • FXR suppresses human liver cancer cell proliferation through the inhibition of the mTOR/S6K signaling pathway.
  • FXR serves as a potential biomarker for assessing personalized mTOR inhibitor treatment strategies in liver cancer patients.
Keywords:
FXRLiver cancer cellsProliferationmTOR/S6K

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