Inhibition of STAT3 signalling contributes to the antimelanoma action of atractylenolide II.

Autor: Fu, Xiu‐Qiong, Chou, Gui‐Xin, Kwan, Hiu Yee, Tse, Anfernee Kai‐Wing, Zhao, Li‐Han, Yuen, Tsz‐Kin, Cao, Hui‐hui, Yu, Hua, Chao, Xiao‐Juan, Su, Tao, Cheng, Brian Chi‐Yan, Sun, Xue‐Gang, Yu, Zhi‐Ling
Předmět:
Zdroj: Experimental Dermatology; Nov2014, Vol. 23 Issue 11, p855-857, 3p
Abstrakt: Our previous studies showed that atractylenolide II ( AT- II) has antimelanoma effects in B16 melanoma cells. In this study, we investigated the involvement of STAT3 signalling in the antimelanoma action of AT- II. Daily administration of AT- II (12.5, 25 mg/kg, i.g.) for 14 days significantly inhibited tumor growth in a B16 xenograft mouse model and inhibited the activation/phosphorylation of STAT3 and Src in the xenografts. In B16 and A375 cells, AT- II (20, 40 μ m) treatment for 48 h dose-dependently reduced protein expression levels of phospho- STAT3, phospho- Src, as well as STAT3-regulated Mcl-1 and Bcl-x L. Overexpression of a constitutively active variant of STAT3, STAT3 C in A375 cells diminished the antiproliferative and apoptotic effects of AT- II. These data suggest that inhibition of STAT3 signalling contributes to the antimelanoma action of AT- II. Our findings shed new light on the mechanism of action underlying the antimelanoma effects of AT- II and provide further pharmacological basis for developing AT- II as a novel melanoma chemopreventive/chemotherapeutic agent. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index