期刊
EXPERIMENTAL DERMATOLOGY
卷 27, 期 2, 页码 201-204出版社
WILEY
DOI: 10.1111/exd.13454
关键词
Cytotoxicity; apoptosis; metastasis; molecular pathways; targeted therapy
类别
资金
- Research Grants Council of Hong Kong [GRF12125116]
- National Natural Science Foundation of China [81673649]
- Natural Science Foundation of Guangdong Province [2016A030313007]
- Science, Technology and Innovation Commission of Shenzhen [JCYJ20140807091945050, JCYJ20150630164505508, JCYJ20160229210327924]
- Hong Kong Baptist University [FRG1/16-17/048, FRG2/16-17/033]
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.
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