Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 437, Issue 4, Pages 550-556Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2013.06.113
Keywords
Celastrol; EMT; E-cadherin; Snail; Invasion
Categories
Funding
- basic science research program through the National Research Foundation of Korea (NRF)
- Ministry of Education [2010-0024893]
- Asan Institute for Life Sciences, Seoul, Korea [2013-529]
- National Research Foundation of Korea [2010-0024893] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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The epithelial mesenchymal transition (EMT) is a pivotal event in the invasive and metastatic potentials of cancer progression. Celastrol inhibits the proliferation of a variety of tumor cells including leukemia, glioma, prostate, and breast cancer; however, the possible role of celastrol in the EMT is unclear. We investigated the effect of celastrol on the EMT. Transforming growth factor-beta 1 (TGF-beta 1) induced EMT-like morphologic changes and upregulation of Snail expression. The downregulation of E-cadherin expression and upregulation of Snail in Madin Darby Canine Kidney (MOCK) and A549 cell lines show that TGF-beta 1-mediated the EMT in epithelial cells; however, celastrol markedly inhibited TGF-beta 1-induced morphologic changes, Snail upregulation, and E-cadherin expression. Migration and invasion assays revealed that celastrol completely inhibited TGF-beta 1-mediated cellular migration in both cell lines. These findings indicate that celastrol downregulates Snail expression, thereby inhibiting TGF-beta 1-induced EMT in MDCK and A549 cells. Thus, our findings provide new evidence that celastrol suppresses lung cancer invasion and migration by inhibiting TGF-beta 1-induced EMT. (C) 2013 Elsevier Inc. All rights reserved.
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