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Department of Molecular Biology, Pusan National University [K-W. K., S-K. B., O-H. L., M-H. B., M-J. L.], and Department of Internal Medicine, Kosin University School of Medicine [B. C. P.], Pusan 609-735, Korea
Insulin-like growth factor II (IGF-II) is highly expressed during hepatocarcinogenesis (P. Schirmacher et al., Cancer Res., 52: 2549–2556, 1992; B. C. Park et al., J. Hepatol., 22: 286–294, 1995). However, the mechanism of its enhanced expression is largely unknown. In this study, we show that IGF-II mRNA levels are increased within six h of exposing human hepatoma cell cultures to hypoxia, suggesting that hypoxia may be a strong stimulus for the induction of IGF-II expression in the process of hepatocarcinogenesis. This finding and the fact that hepatocellular carcinoma (HCC) is a typical hypervascular tumor (M. Mise et al., Hepatology, 23: 455–464, 1996) imply that IGF-II may play an important role in the development of neovascularization of HCC. Here we demonstrate that IGF-II substantially increases vascular endothelial growth factor (VEGF) mRNA and protein levels in a time-dependent manner in human hepatoma cells. The induction of VEGF by IGF-II was additively increased by hypoxia. Moreover, the direct angiogenic activity of IGF-II was observed in the quantitative chick chorioallantoic membrane assay (M. Nguyen et al., Microvasc. Res., 47: 31–40, 1994). These data suggest that IGF-II may be a hypoxia-inducible angiogenic factor in HCC.
1 This work was supported by the Cancer Research Grant from the Ministry of Health and Welfare and the Korea Science and Engineering Foundation (KOSEF) through the Cancer Research Center at Seoul National University, Korea.
2 To whom requests for reprints should be addressed. Fax: 82-51-513-9258; E-mail: kimkw@hyowon.cc.pusan.ac.kr.
Received 7/23/97. Accepted 11/11/97.
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