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Updated: May 9, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

Celastrol inhibits TGF-β1-induced epithelial-mesenchymal transition by inhibiting Snail and regulating E-cadherin

Hyereen Kang1, Minjae Lee, Sung-Wuk Jang

  • 1Department of Biomedical Sciences, University of Ulsan College of Medicine, Seoul, Republic of Korea.

Biochemical and Biophysical Research Communications
|July 16, 2013
PubMed

Insights

Celastrol inhibits cancer cell migration and invasion by blocking the epithelial-mesenchymal transition (EMT). This compound suppresses key EMT markers, offering a potential therapeutic strategy for advanced cancers.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Medicine

Background:

  • The epithelial-mesenchymal transition (EMT) is crucial for cancer cell invasion and metastasis.
  • Celastrol is known to inhibit tumor cell proliferation, but its role in EMT was unexplored.

Purpose of the Study:

  • To investigate the effect of celastrol on TGF-β1-induced EMT.
  • To determine if celastrol can inhibit cancer cell migration and invasion by targeting EMT.

Main Methods:

  • Utilized Madin-Darby Canine Kidney (MDCK) and A549 cell lines to study EMT.
  • Administered transforming growth factor-beta 1 (TGF-β1) to induce EMT.
  • Assessed changes in cell morphology, E-cadherin and Snail expression, and cell migration/invasion.

Main Results:

  • TGF-β1 induced EMT-like changes, including Snail upregulation and E-cadherin downregulation.
  • Celastrol significantly inhibited TGF-β1-induced morphological changes and Snail upregulation.
  • Celastrol completely blocked TGF-β1-mediated cell migration and invasion, and restored E-cadherin expression.

Conclusions:

  • Celastrol effectively inhibits TGF-β1-induced EMT in epithelial cells.
  • Celastrol suppresses cancer cell invasion and migration by downregulating Snail expression.
  • Celastrol demonstrates potential as an anti-metastatic agent in lung cancer treatment.
Keywords:
CelastrolE-cadherinEMTInvasionSnail

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