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

Xiuqiong FU, Gui Xin Chou, Hiu Yee KWAN, Anfernee K W TSE, Li Han Zhao, Tsz Kin Yuen, Hui Hui Cao, Hua Yu, Xiao Juan Chao, Tao Su, Brian Chi Yan Cheng, Xue Gang Sun, Zhiling YU*

*Corresponding author for this work

Research output: Contribution to journalLetterpeer-review

19 Citations (Scopus)

Abstract

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 μm) treatment for 48 h dose-dependently reduced protein expression levels of phospho-STAT3, phospho-Src, as well as STAT3-regulated Mcl-1 and Bcl-xL. Overexpression of a constitutively active variant of STAT3, STAT3C 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.

Original languageEnglish
Pages (from-to)855-857
Number of pages3
JournalExperimental Dermatology
Volume23
Issue number11
DOIs
Publication statusPublished - 1 Nov 2014

Scopus Subject Areas

  • Biochemistry
  • Molecular Biology
  • Dermatology

User-Defined Keywords

  • Atractylenolide II
  • Melanoma
  • Src
  • STAT3

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