Scharf J G, Dombrowski F, Ramadori G
Department of Medicine, Division of Gastroenterology and Endocrinology, Georg-August-Universität, D-37075 Göttingen, Germany.
Mol Pathol. 2001 Jun;54(3):138-44. doi: 10.1136/mp.54.3.138.
Deregulation of the insulin-like growth factor (IGF) axis, including the autocrine production of IGFs, IGF binding proteins (IGFBPs), IGFBP proteases, and the expression of the IGF receptors, has been identified in the development of hepatocellular carcinoma (HCC). Characteristic alterations detected in HCC and hepatoma cell lines comprise the increased expression of IGF-II and the IGF-I receptor (IGF-IR), which have emerged as crucial events in malignant transformation and the growth of tumours. Alterations of IGFBP production and the proteolytic degradation of IGFBPs resulting in an excess of bioactive IGFs, as well as the defective function of the IGF degrading IGF-II/mannose 6-phosphate receptor (IGF-II/M6PR), may further potentiate the mitogenic effects of IGFs in the development of HCC.
胰岛素样生长因子(IGF)轴的失调,包括IGF的自分泌产生、IGF结合蛋白(IGFBP)、IGFBP蛋白酶以及IGF受体的表达,已在肝细胞癌(HCC)的发生发展中被发现。在HCC和肝癌细胞系中检测到的特征性改变包括IGF-II和IGF-I受体(IGF-IR)表达增加,这已成为恶性转化和肿瘤生长中的关键事件。IGFBP产生的改变以及IGFBP的蛋白水解降解导致生物活性IGF过量,以及降解IGF-II/甘露糖6-磷酸受体(IGF-II/M6PR)功能缺陷,可能进一步增强IGF在HCC发生发展中的促有丝分裂作用。