| Summary: | 碩士 === 國立成功大學 === 藥理學研究所 === 101 === Hepatocellular carcinoma (HCC) is a type of tumor that results from chronic inflammation triggered by hepatotropic viruses, alcoholism or other toxic chemicals. Constitutive activation of nuclear factor-kB (NF-kB) is an important event involved in chronic inflammation of liver. CPAP (Centrosomal protein P4.1-associated protein), which plays an important role in centrosomal functions, is previously
identified as a transcriptional co-activator of NF-kB. In addition, it was reported that the HBV X protein (HBx) of hepatitis B virus (HBV) can enhance the activation of NF-kB. In this study, we demonstrated that overexpression of GFP-CPAP synergistically increases the HBx-mediated NF-kB transcriptional activity, whereas knockdown expression of CPAP by siRNA attenuates this effect. Immunoprecipitation assay showed that CPAP interacts with HBx. Interestingly,
HBx enhances the promoter activity of CPAP may be through the interaction with cyclic adenosine monophosphate response element-binding protein (CREB). Stably expression of CPAP in HCC cell lines increased the cell proliferation ability. Taken together, our results indicate that CPAP can cooperate with HBx to increase the NF-kB activity, which may contribute to hepatocarcinogenesis.
|
|---|
