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C7 peptide inhibits hepatocellular carcinoma metastasis by targeting the HGF/c-Met signaling pathway.

Authors
  • Zhao, Mingyuan1
  • Wang, Yinhe1, 2
  • Liu, Yan1
  • Zhang, Wanchun1, 2
  • Liu, Yakun1
  • Yang, Xiaoming3
  • Cao, Yunxia1, 2
  • Wang, Siying1
  • 1 Department of Pathophysiology, Anhui Medical University , Hefei , Anhui , P. R. China. , (China)
  • 2 Department of Gynaecology and Obstetrics, The First Affiliated Hospital of Anhui Medical University , Hefei , Anhui , P. R. China. , (China)
  • 3 State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics , Beijing , P. R. China. , (China)
Type
Published Article
Journal
Cancer Biology & Therapy
Publisher
Landes Bioscience
Publication Date
Jan 01, 2019
Volume
20
Issue
12
Pages
1430–1442
Identifiers
DOI: 10.1080/15384047.2019.1647051
PMID: 31441380
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Hepatocellular carcinoma (HCC), characterized by a high rate of metastasis and recurrence after surgery, is caused by malignant proliferation of hepatocytes with epigenetic and/or genetic mutations. In particular, abnormal activation of the hepatocyte growth factor (HGF)-/c-mesenchymal-epithelial transition receptor (c-Met) axis is closely associated with HCC metastasis. Unfortunately, effective treatments or drugs that target the HGF/c-Met signaling pathway are still in the research pipeline. Here, a c-Met inhibitor named the C7 peptide, which can inhibit both HGF and c-Met, can significantly inhibit HGF-induced (but not EGF-induced) cell migration and suppress the phosphorylation of c-Met, Akt and Erk1/2. Moreover, the C7 peptide can also significantly suppress tumor metastasis in nude mice and the phosphorylation of c-Met. Together, our current findings, demonstrated that the C7 peptide can inhibit HGF-induced cancer cell migration and invasion through the inhibition of Akt and Erk1/2. Identification of a peptide that can block HGF/c-Met signaling provides new insight into the mechanism of HCC and future clinical treatments.

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