Hepatocyte growth factor promotes hepatocarcinogenesis through c-Met autocrine activation and enhanced angiogenesis in transgenic mice treated with diethylnitrosamine
Hepatocyte growth factor promotes hepatocarcinogenesis through c-Met autocrine activation and enhanced angiogenesis in transgenic mice treated with diethylnitrosamine
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DOI：
10.1038/sj.onc.1205248
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发表时间：
2002-03-14
期刊：
影响因子：
8
通讯作者：
Mori, M
中科院分区：
文献类型：
--
作者：
Horiguchi, N;Takayama, H;Mori, M
肝细胞生长因子（HGF）是肝细胞的有丝分裂原，但目前尚不清楚HGF是否刺激或抑制肝癌发生。我们先前曾报道，金属硫蛋白基因启动子下的肝细胞生长因子转基因小鼠自发发展良性和恶性肝肿瘤后，17个月的年龄。为了阐明肝细胞生长因子在肝癌发生中的作用，对肝细胞生长因子转基因小鼠给予二乙基亚硝胺（DEN）。HGF过度表达加速DEN诱导的肝癌发生，通常伴有异常血管形成。在这项研究中，59%的转基因雄性（野生型雄性为20%）和39%的转基因雌性（野生型雌性为2%）在48周时发生了良性或恶性肝脏肿瘤（P
Hepatocyte growth factor (HGF) is a mitogen for hepatocytes, but it is not clear whether HGF stimulates or inhibits hepatocarcinogenesis. We previously reported that HGF transgenic mice under the metallothionein gene promoter developed benign and malignant liver tumors spontaneously after 17 months of age. To elucidate the role of HGF in hepatocarcinogenesis, diethylnitrosamine (DEN) was administered to HGF transgenic mice. HGF overexpression accelerated DEN-induced hepatocarcinogenesis, often accompanied by abnormal blood vessel formation. In this study, 59% of transgenic mates (versus 20% of wild-type males) and 39% of transgenic females (versus 2% of wild-type females) developed either benign or malignant liver tumors by 48 weeks (P