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Activation of FXR Suppresses Esophageal Squamous Cell Carcinoma Through Antagonizing ERK1/2 Signaling Pathway

Qingqing Feng1, Hongli Zhang1, Denglin Yao1

  • 1State Key Laboratory of Chemical Resource Engineering, College of Life Science and Technology, Beijing University of Chemical Technology, Beijing, People's Republic of China.

Cancer Management and Research
|August 9, 2021
PubMed
Abstract

Insights

Activating the farnesoid X receptor (FXR) inhibits esophageal squamous cell carcinoma (ESCC) growth by reducing proliferation and migration. This FXR activation also suppresses tumor development and key signaling pathways involved in ESCC progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Farnesoid X receptor (FXR) is a nuclear receptor regulating homeostasis and suppressing cancer.
  • FXR's role in esophageal squamous cell carcinoma (ESCC) was previously unknown.

Purpose of the Study:

  • To investigate the role of FXR activation in the progression of ESCC.
  • To evaluate FXR as a potential therapeutic target for ESCC.

Main Methods:

  • In vitro studies using ESCC cell lines (KYSE150, EC109) treated with FXR ligand GW4064.
  • In vivo studies using a xenograft mouse model to assess GW4064 effects on tumor growth.
  • Analysis of cell proliferation, migration, apoptosis, cell cycle, and ERK1/2 signaling pathway activity.

Main Results:

  • GW4064 inhibited ESCC cell proliferation and migration, induced apoptosis, and caused cell cycle arrest.
  • FXR activation reduced ERK1/2 phosphorylation, a key pathway in cancer progression.
  • GW4064 suppressed ESCC tumor growth in vivo and decreased ERK1/2 phosphorylation in tumors.

Conclusions:

  • FXR activation demonstrates anti-cancer effects in ESCC.
  • Targeting FXR may represent a promising therapeutic strategy for esophageal squamous cell carcinoma.
  • FXR activation could be a valuable adjuvant therapy for ESCC treatment.
Keywords:
ERK1/2ESCCFXRGW4064farnesoid X receptor

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