Celastrol inhibits cancer metastasis by suppressing M2-like polarization of macrophages
Journal Article
·
· Biochemical and Biophysical Research Communications
- Hangzhou Xuejun High School (China)
- College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058 (China)
- Department of Pharmacy, The Second Affiliated Hospital, Zhejiang University, Hangzhou, 310006 (China)
Highlights: • Celastrol inhibited M2-like polarization of macrophages. • Celastrol intervened STAT6 signaling pathway. • Celastrol is a potential agent for cancer metastasis treatment. In recent years, a large amount of clinical and experimental data has shown that M2-like polarized tumor-associated macrophages (TAMs) play an important role in cancer metastasis. Therefore, TAMs, especially M2-like TAMs is a promising target for anti-tumor metastasis therapy. Here, we found that celastrol dose-dependently suppressed IL-13 induced CD206 expression both in RAW264.7 and in primary macrophages. Consistently, celastrol also inhibited the expression of M2-like specific genes, including MRC1, Arg1, Fizz1, Mgl2 and CD11c. Further, by the employment of 4T1 breast cancer model, we found that celastrol significantly prevented cancer metastasis in vivo. Mechanistically, celastrol completely ameliorated STAT6 phosphorylation, which is the key signal molecule responsible for M2 polarization. Our research puts forward a new application of celastrol in anti-cancer metastasis, by intervening M2-like polarization through inhibiting STAT6.
- OSTI ID:
- 23105629
- Journal Information:
- Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 2 Vol. 503; ISSN 0006-291X; ISSN BBRCA9
- Country of Publication:
- United States
- Language:
- English
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