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.

中文翻译：

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C7肽通过靶向HGF / c-Met信号通路来抑制肝癌的转移。

肝细胞癌（HCC）的特征是手术后转移和复发率很高，是由具有表观遗传和/或基因突变的肝细胞恶性增殖引起的。特别地，肝细胞生长因子（HGF）-/ c-间质-上皮转化受体（c-Met）轴的异常激活与HCC转移密切相关。不幸的是，靶向HGF / c-Met信号通路的有效疗法或药物仍在研究中。在这里，一种名为C7肽的c-Met抑制剂可同时抑制HGF和c-Met，可显着抑制HGF诱导的（但不是EGF诱导的）细胞迁移，并抑制c-Met，Akt和Erk1 /的磷酸化。 2。此外，C7肽还可以显着抑制裸鼠的肿瘤转移和c-Met的磷酸化。一起，我们目前的发现表明，C7肽可以通过抑制Akt和Erk1 / 2来抑制HGF诱导的癌细胞迁移和侵袭。可以阻断HGF / c-Met信号传导的肽的鉴定为HCC的机制和未来的临床治疗提供了新的见识。