Effects Of Hepatitis B Virus On Oncogenes, MMPs And TIMPs

Hepatits B virus(HBV)infection was the most important risk of high occurrence of hepatocellular carinoma(HCC)in china.Establishment of available HBV infected model was an accessible method for vial pathogenesis research. Previously,we had successfully established HpG2 cell line RHBV-3 in which HBV can replicate and express specific antigens,and simultaneously obtained the control cell RepSal-1.These cell lines accommodated with us a path for assessing the effects of HBV replication on cell genes。Proto-oncogenes were involved in normal cell function,and in certain case their mutation or aberrant activation in the cell was associated with tumor formation。Now there were several lines of evidence suggest that HBV may lead directly to HCC by evoking oncogenic potential of HBV through chromosomal integration(cisactivation) or transactivation of cellular genes.Further more,the relationships between matrix metalloproteinases(MMPs),tissue inhibitors of metalloproteinases(TIMPs)and the invasion and metastasis of hepatocellular carcinoma(HCC)were in focus。It was reported that expression of MMP9 increased not only in Hep3B cell in which HBV integrated but in hepatocyte which HBV transfected。However,effects of TIMPs did not reported。Thus,The aim of this study was to preliminary assess the oncogenic potential of hepatitis B virus by anlysing the expression of proto-oncogenes,MMPs,TIMPs of RHBV-3 cell。In the first part of this study we used specific primers for Real-time Quantitative Polymerase Chain Reaction to anlysed the transcriptions of Ras,Jun,Myc,Fos,MMP2,9 and TIMP 1-4。Quantitative RT-PCR showed that HBV replication enhance the transcriptions of Ras,Jun,Myc,MMP2,9,TIMP1,3,but inhibit the transcription of TIMP4。In the second part of this study Gelatin Zymography revealed that the HBV replication promoted the expression as well as the activation of MMP2 and MMP9。 Reverse Gelatin Zymography demonstrated that HBV replication could promoted the expressions of TIMP1 and TIMP3 but inhibit ed those of TIMP4。In conclusion,the replication of HBV could enhance theteanscript levers of oncogenes.But then the effects on the expressions of MMPs and TIMPs were sophisticated。...