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G Protein–Coupled Receptors (GPCRs) are membrane-bound receptors that transiently associate with heterotrimeric G proteins and induce an appropriate response to various stimuli. GPCRs regulate critical physiological pathways and are excellent drug targets for treating diseases such as diabetes, cancer, obesity, depression, or Alzheimer's. Nearly 35% of approved drugs implement their therapeutic effects by selectively interacting with specific GPCRs.
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Liver Regeneration01:24

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Updated: Apr 19, 2026

Reverse Yeast Two-hybrid System to Identify Mammalian Nuclear Receptor Residues that Interact with Ligands and/or Antagonists
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FXR and liver carcinogenesis.

Xiong-fei Huang1, Wei-yu Zhao2, Wen-dong Huang2

  • 11] Department of Pathology and Institute of Oncology, Preclinical School, Fujian Medical University, Fuzhou 350004, China [2] Key Laboratory of Ministry of Education for Gastrointestinal Cancer, Fujian Medical University, Fuzhou 350004, China.

Acta Pharmacologica Sinica
|December 16, 2014
PubMed
Summary
This summary is machine-generated.

Farnesoid X receptor (FXR) acts as a liver tumor suppressor by maintaining metabolic balance, promoting repair, and regulating genes. Reactivating FXR may offer a therapeutic strategy for liver cancer.

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Area of Science:

  • Hepatology
  • Molecular Biology
  • Oncology

Background:

  • Farnesoid X receptor (FXR) is a nuclear receptor and transcription factor crucial for liver function.
  • FXR is recognized for its roles in protecting liver cells and suppressing tumor development.

Purpose of the Study:

  • To elucidate the multifaceted mechanisms by which FXR suppresses liver carcinogenesis.
  • To explore the potential of FXR reactivation as a therapeutic strategy for liver cancer.

Main Methods:

  • Review and synthesis of existing literature on FXR's role in liver metabolism, regeneration, cell survival, inflammation, and gene regulation in the context of cancer.
  • Analysis of pathways involving bile acid, glucose, and lipid metabolism.
  • Investigation of FXR's influence on cell death, survival, inflammation, tumor-suppressor genes, and oncogenes.

Main Results:

  • FXR maintains normal liver metabolism (bile acids, glucose, lipids) and promotes liver regeneration and repair.
  • FXR enhances hepatocyte survival, protects against cell death, and suppresses hepatic inflammation.
  • FXR directly upregulates tumor-suppressor genes and downregulates oncogenes, thereby inhibiting liver carcinogenesis.
  • Inflammation and epigenetic silencing can reduce FXR expression during tumor development.

Conclusions:

  • FXR functions as a multi-faceted liver protector and tumor suppressor through diverse mechanisms.
  • The therapeutic reactivation of FXR holds promise as a novel strategy for treating liver cancer.