Unexpectedly, some of the tumor endothelium was positive for anti-rat CD34, whereas the counterpart could form neither tumors nor tube-like structures. Wnt/β-catenin expression in Bmi1high oval cells was 2 folds that of the control. Their Notch1 expression, however, was 3 times higher. After silencing notch1 expression, the tube forming capacity was significantly impaired. Conclusion: Bmi1 up-regulated oval cells may be capable of hepatocarcinogenesis by enhancing Wnt/β-catenin expression, and tube formation in vitro and endothelial
transdifferentiation in vivo by Notch1 expression, respectively. Figure1. rCD34 (A) and mCD34 (B) positive endothelium (transverse arrow); Bmi1, Wnt and Notch1 expression (RT-PCR) in oval cells (C); tube formation assay, this website D: Bmi1 high; E: control ; F: Notch1-siRNA;G: HUVECs. Disclosures: The following people have nothing to disclose: Mansheng Zhu, Rui Zhang, Wen-rui Napabucasin molecular weight Wu, Hong Zeng, Xiujing Yue, Lei-bo Xu, Chao Liu Background: Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide. Approximately 564,000 individuals are expected to be diagnosed with HCC per year. HCC is especially frequent in Asia due to a high prevalence of chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. In China, HCC has been ranked as the second most frequent fatal cancer since the 1990s, and the majority of HCCs
in China are caused by HBV infection. The aim of this study Rho was to identify disease-related host proteins, which may be useful targets for future therapeutic protocols. Methods: To identify the proteins involved in HCC carcinogenesis and novel therapeutic targets, we used iTRAQ and mass spectrometry analysis to study the differentially expressed proteins in tumor and adjacent non-tumor tissue samples. Samples from 9 hepatitis B virus-associated HCC patients were analyzed. Results: In total,
1 607 unique proteins were identified and 222 proteins were found to be differentially expressed in tumor samples compared with that in non-tumor samples. Several differentially expressed proteins were further validated by real-time quantitative RT-PCR, Western Blot and immunohistochemical analysis. Functional analysis of glucose-6-phosphate dehydrogenase(G6PD), one of the highly expressed proteins in tumor samples, was carried out with small interfering (si)RNA-based silencing transfection methods. siRNA-mediated G6PD silencing reduced HBV replication by nearly 5-fold through the interferon (IFN) signaling pathway. Furthermore, silencing G6PD expression suppressed the migration and invasion of HCC cells in vitro. Conclusion: In summary, our results provide information on the mechanism of HCC development, and suggest that suppression of the G6PD expression may be a promising strategy in the development of novel cancer therapeutic drugs.