Objective：To explore the role of proline hydroxylase 2 (PHD2) in hepatocellular carcinoma angiogenesis.
Methods：(1)SP method immunohistochemical staining was used to detect PHD2 and microvessel density (MVD) was identified in 72 hepatocellular carcinoma tissues. Clinicopathological and microvessel density data were analysed. (2)Microvascular endothelial (HMEC-1) cell line was cultured in vitro, then, the cell lines were treated with different concentrations of cobalt chloride (treatment group). The expression level of  PHD2 protein was detected by Western blot. Tube formation capability of HMEC-1 cell in matrigel was examined.
Results：The expression positive rate of PHD2  in  HCC tissues was significantly lower than that in peritumor liver tissues and normal liver tissue ［22.2%（16/72）, 68.1%（49/72）, 84.6%（11/13）, respectively］(P＜0.05). MVD in PHD2 higer expression group was lower than in PHD2 low expression (52.1±4.3 vs. 69.2±5.5  respectively)(P＜0.05). Compared with the control group (normal liver tissues), the protein level of PHD2 and HIF-1α was decreased significantly,  the protein level of VEGF was increased significantly, tube formation capability of HMEC-1 cell in matrigel were decreased after CoCl2 treatment (P＜0.05).
Conclusions： In hypoxic microenvironment, the expression of PHD2 is decreased and endothelial cell proliferation is increased, but tube formation capability of endothelial cell is decreased, leading to decrease vascular maturity in HCC tumor  which are the important factors to promote invasion and metastasis of HCC.