C7 peptide inhibits hepatocellular carcinoma metastasis by targeting the HGF/c-Met signaling pathway. Issue 12 (2nd December 2019)

• Record Type: Journal Article
• Authors: Zhao, Mingyuan; Wang, Yinhe; Liu, Yan; Zhang, Wanchun; Liu, Yakun; Yang, Xiaoming; Cao, Yunxia; Wang, Siying
• Is Part Of: Cancer biology & therapy. Volume 20:Issue 12(2019)
• Page Start: 1430
• Page End: 1442
• Publication Date: 2019-12-02
• Subjects: C7 peptide -- hepatocellular carcinoma (HCC) -- HGF/c-Met axis -- migration -- invasion; 616.99406
• DOI: 10.1080/15384047.2019.1647051
• Languages: English
• ISSNs: 1538-4047

Abstract

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.