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The JAK 2/ STAT 3 pathway is involved in the anti‐melanoma effects of atractylenolide I
Author(s) -
Fu XiuQiong,
Chou JiYao,
Li Ting,
Zhu PeiLi,
Li JunKui,
Yin ChengLe,
Su Tao,
Guo Hui,
Lee KinWah,
Hossen Muhammad Jahangir,
Chou GuiXin,
Yu ZhiLing
Publication year - 2018
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.13454
Subject(s) - stat3 , apoptosis , chemistry , melanoma , jak stat signaling pathway , signal transduction , stat , cancer research , pharmacology , biochemistry , biology , tyrosine kinase
In this study, we aimed to investigate the anti‐melanoma effects and the JAK 2/ STAT 3 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‐ JAK 2 and phospho‐ STAT 3, and in turn downregulated the mRNA levels of STAT 3‐targeted genes, including Bcl‐ xL , MMP ‐2 and MMP ‐9. Furthermore, the cytotoxic effect of atractylenolide I was attenuated in STAT 3‐overactivated A375 cells. These findings indicate that inhibition of JAK 2/ STAT 3 signalling contributes to the anti‐melanoma effects of atractylenolide I.