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

Exp Dermatol. 2018 Feb;27(2):201-204. doi: 10.1111/exd.13454. Epub 2018 Jan 5.

Abstract

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.

Keywords: Cytotoxicity; apoptosis; metastasis; molecular pathways; targeted therapy.

Publication types

  • Letter
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis*
  • Cell Line, Tumor
  • Cell Movement
  • Cell Survival
  • Down-Regulation
  • Gene Expression Profiling
  • Humans
  • Janus Kinase 2 / metabolism*
  • Lactones / pharmacology*
  • Melanoma / metabolism*
  • Phosphorylation
  • RNA, Messenger / metabolism
  • STAT3 Transcription Factor / metabolism*
  • Sesquiterpenes / pharmacology*
  • Signal Transduction / drug effects
  • Skin Neoplasms / metabolism*

Substances

  • Lactones
  • RNA, Messenger
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Sesquiterpenes
  • atractylenolide I
  • JAK2 protein, human
  • Janus Kinase 2