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Biochem Biophys Res Commun. 2018 Sep 5;503(2):414-419. doi: 10.1016/j.bbrc.2018.03.224. Epub 2018 Jun 29.

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

Author information

1
Hangzhou Xuejun High School, PR China.
2
College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, PR China.
3
Department of Pharmacy, The Second Affiliated Hospital, Zhejiang University, Hangzhou, 310006, PR China.
4
College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, PR China. Electronic address: pharma12@zju.edu.cn.

Abstract

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.

KEYWORDS:

Cancer metastasis; Celastrol; Macrophage; Polarization

PMID:
29614269
DOI:
10.1016/j.bbrc.2018.03.224
[Indexed for MEDLINE]
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