摘要
Constitutive activation of the insulin-like growth factor (IGF)-signaling axis is frequently observed in human hepatocellular carcinoma(HCC).Especially the over- expression of the fetal growth factor IGF-Ⅱ,IGF-Ⅰ receptor(IGF-IR),and cytoplasmic downstream effectors such as insulin-receptor substrates(IRS)contribute to proliferation,anti-apoptosis,and invasive behavior. This review focuses on the relevant alterations in this signaling pathway and independent in vivo models that support the central role IGF-Ⅱsignaling during HCC development and progression.Since this pathway has become the center of interest as a target for potential anti-cancer therapy in many types of malignancies,various experimental strategies have been developed,including neutralizing antibodies and selective receptor kinase inhibitors,with respect to the specific and efficient reduction of oncogenic IGF-Ⅱ/IGF-IR-signaling.
Constitutive activation of the insulin-like growth factor （IGF）-signaling axis is frequently observed in human hepatocellular carcinoma （HCC）. Especially the overexpression of the fetal growth factor IGF-Ⅱ, IGF-Ⅰ receptor （IGF-IR）, and cytoplasmic downstream effectors such as insulin-receptor substrates （IRS） contribute to proliferation, anti-apoptosis, and invasive behavior. This review focuses on the relevant alterations in this signaling pathway and independent in vivo models that support the central role IGF-Ⅱ signaling during HCC development and progression. Since this pathway has become the center of interest as a target for potential anti-cancer therapy in many types of malignancies, various experimental strategies have been developed, including neutralizing antibodies and selective receptor kinase inhibitors, with respect to the specific and efficient reduction of oncogenic IGF- Ⅱ/IGF-IR-signaling.
关键词
肝细胞癌
类胰岛素生长因子
胰岛素受体
治疗方法
Hepatocellular carcinoma
Insulin-like growth factor-Ⅱ
Insulin-like growth factor-Ⅰ receptor
Insulin receptor substrate
House models
Therapy
