Our and others’ studies have indicated that HIF-1α played a vital role for the angiogenesis and VM under hypoxia [11, 26–28]. To determine the origin of the change in VEGF and Flk-1 expression, we used the Sirolimus to inhibit the activity of HIF-1α. Sirolmus, known as rapamycin, is proved to be as the inhibitor of HIF-1α [26, 29, 30]. Consistent with other researches, the changes in the expression of VEGF, Flk-1 and

Cyclin D1 were PI3K inhibitor HIF-1α transcriptional dependent [10, 31]. However, the change in the expression of p53 was HIF-1α transcriptional independent. Conclusion In summary, the ovarian cancer cells could be induced into ELs which seemed similarly to progenitor endothelial cells by hypoxia. After induced, the ELs would get some characteristics of endothelial cells

and would lose some malignant characteristics of the original cancer cells. The increased expression of HIF-1a, and HIF-1α depended VEGF and Flk-1 might contribute to the VM and the vasculogenesis. During the transition, HIF-1α took an important role in the molecular mechanisms, while there still has other HIF-1α-independent mechanism in this process. Acknowledgements This study was STA-9090 clinical trial supported by National Natural Science Foundation of China grants 30471806, 30470689 and 30900716, Postdoctoral Science Foundation of China grant 20040350454, and Science and Technology Commission of Shanghai Municipalitygrant 04JC14021. References 1. Huang S, Robinson JB, Deguzman A, Bucana CD, Fidler IJ: Blockade of nuclear AZD1480 in vivo factor-kappaB signaling inhibits angiogenesis and tumorigenicity of human ovarian cancer cells by suppressing expression of vascular endothelial

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