The JAK2/STAT3 pathway is involved in the anti-melanoma effects of atractylenolide I

被引：56
作者：
Fu, Xiu-Qiong [1 ]
Chou, Ji-Yao [1 ]
Li, Ting [1 ]
Zhu, Pei-Li [1 ]
Li, Jun-Kui [1 ]
Yin, Cheng-Le [1 ]
Su, Tao [1 ]
Guo, Hui [1 ]
Lee, Kin-Wah [1 ]
Hossen, Muhammad Jahangir [1 ]
Chou, Gui-Xin [2 ]
Yu, Zhi-Ling [1 ,3 ]
机构：
[1] Hong Kong Baptist Univ, Ctr Canc & Inflammat Res, Sch Chinese Med, Hong Kong, Hong Kong, Peoples R China
[2] Shanghai Univ Tradit Chinese Med, Inst Chinese Mat Med, Shanghai, Peoples R China
[3] HKBU Shenzhen Res Inst & Continuing Educ, Res & Dev Ctr Nat Hlth Prod, Shenzhen, Peoples R China
来源：
EXPERIMENTAL DERMATOLOGY | 2018年 / 27卷 / 02期
基金：
中国国家自然科学基金;
关键词：
Cytotoxicity; apoptosis; metastasis; molecular pathways; targeted therapy; MELANOMA-CELLS; STAT3;
D O I：
10.1111/exd.13454
中图分类号：
R75 [皮肤病学与性病学];
学科分类号：
100206 ;
摘要：
In this study, we aimed to investigate the anti-melanoma effects and the JAK2/STAT3 pathway-related mechanism of action of atractylenolide I in human melanoma cells. Our results showed that atractylenolide I effectively reduced viability, induced apoptosis and inhibited migration of melanoma cells. Meanwhile, atractylenolide I decreased the protein expression levels of phospho-JAK2 and phospho-STAT3, and in turn downregulated the mRNA levels of STAT3-targeted genes, including Bcl-xL, MMP-2 and MMP-9. Furthermore, the cytotoxic effect of atractylenolide I was attenuated in STAT3-overactivated A375 cells. These findings indicate that inhibition of JAK2/STAT3 signalling contributes to the anti-melanoma effects of atractylenolide I.
引用
收藏
页码：201 / 204
页数：4
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