4.6 Article

Scutellarin suppresses migration and invasion of human hepatocellular carcinoma by inhibiting the STAT3/Girdin/Akt activity

期刊

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2016.12.114

关键词

Akt; Girdin; Hepatocellular carcinoma; Invasion; Scutellarin; STAT3

资金

  1. National Natural Science Foundation of China [81360360, 81660399]
  2. Yunnan Provincial Applied Fundamental Research [2013FB149, 2012FB057]
  3. Yunnan Provincial Engineering Research Center of Major Surgical Diseases
  4. Innovative Research Team Project of Yunnan Institutions of Higher Education
  5. Innovative Research Team Project of Yunnan Province [2015HC033]
  6. Yunnan Provincial Academician Workstation of Xiaoping Chen
  7. Breeding Program for Major Scientific and Technological Achievements of Kunming Medical University [CGYP201607]
  8. Medical Leading Talent Project of Yunnan Province
  9. Kunming Medical University [2016D03]

向作者/读者索取更多资源

Scutellarin is an active flavone from Erigeron breviscapine (vant) Hand Mass. This study aimed to investigate the potential role of scutellarin in migration and invasion of human hepatocellular carcinoma (HCC) cells and its possible mechanism. In comparison with the vehicle-treated controls, treatment with scutellarin (50 mg/kg/day) for 35 days significantly mitigated the lung and intrahepatic metastasis of HCC tumors in vivo. Scutellarin treatment significantly reduced HepG2 cell viability in a dose-dependent manner, and inhibited migration and invasion of HCC cells in vitro. Scutellarin treatment significantly reduced STAT3 and Girders of actin filaments (Girdin) expression, STAT3 and Akt phosphorylation in HCC cells. Introduction of STAT3 overexpression restored the scutellarin-downregulated Girdin expression, Akt activation, migration and invasion of HCC cells. Furthermore, induction of Girdin overexpression completely abrogated the inhibition of scutellarin on the Akt phosphorylation, migration and invasion of HCC cells. Scutellarin can inhibit HCC cell metastasis in vivo, and migration and invasion in vitro by downregulating the STAT3/Girdin/Akt signaling. (C) 2016 Elsevier Inc. All rights reserved.

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