Celastrol inhibits cancer metastasis by suppressing M2-like polarization of macrophages

Related Experiment Video

Updated: Feb 12, 2026

Macrophage Differentiation and Polarization into an M2-Like Phenotype using a Human Monocyte-Like THP-1 Leukemia Cell Line
06:38

Macrophage Differentiation and Polarization into an M2-Like Phenotype using a Human Monocyte-Like THP-1 Leukemia Cell Line

Published on: August 2, 2021

31.6K

Yuening Yang1, Shuyuan Cheng2, Guikai Liang2

  • 1Hangzhou Xuejun High School, PR China.

Biochemical and Biophysical Research Communications
|April 4, 2018
PubMed

Insights

Celastrol inhibits M2-like tumor-associated macrophages (TAMs) polarization by blocking STAT6 signaling. This finding presents celastrol as a potential therapeutic agent to prevent cancer metastasis.

Area of Science:

  • Immunology
  • Oncology
  • Pharmacology

Background:

  • M2-like tumor-associated macrophages (TAMs) promote cancer metastasis.
  • Targeting M2-like TAMs is a promising strategy for anti-cancer metastasis therapy.

Purpose of the Study:

  • To investigate the effect of celastrol on M2-like TAM polarization.
  • To explore the potential of celastrol as an anti-metastasis agent.

Main Methods:

  • Celastrol's effect on IL-13 induced CD206 expression in macrophages was assessed.
  • M2-like specific gene expression (MRC1, Arg1, Fizz1, Mgl2, CD11c) was analyzed.
  • The 4T1 breast cancer metastasis model was used to evaluate celastrol in vivo.
  • STAT6 phosphorylation was measured to understand the mechanism of action.

Main Results:

  • Celastrol suppressed IL-13 induced CD206 expression and M2-like specific genes in macrophages.
  • Celastrol significantly inhibited cancer metastasis in the 4T1 breast cancer model.
  • Celastrol ameliorated STAT6 phosphorylation, a key mediator of M2 polarization.

Conclusions:

  • Celastrol effectively inhibits M2-like TAM polarization by targeting STAT6 signaling.
  • Celastrol demonstrates potential as a therapeutic agent for preventing cancer metastasis.
Keywords:
Cancer metastasisCelastrolMacrophagePolarization

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