FAT10Regulates Radiosensitivity In Hepatoma Carcinoma Through MiR-34a

Objective:Reduce the expression of FAT10in HepG2and MHCC-97H cells by smallinterference RNA(siRNA) and detect the variation of the expression of miR-34a andradiosensitivity to confirm that FAT10influences the radiosensitivity ofhepatocellular carcinoma cells via miR-34a.Methods:1.Transfect the siRNA aimed at FAT10into HepG2and MHCC-97H cells,anddetect the expression of FAT10mRNA and protein by qRT-PCR and western blot.2.The bunches of cells divided into six groups：control，siRNA(－),FAT10-siRNA, IR,IR＋siRNA(－),IR＋FAT10-siRNA. The Expression of miR-34awas estimated by qRT-PCR while western-blot was used to detect the protein of Bcl-2and Bax.3. Draw cell growth curves and analyze the cell growth cycles and apoptosis bythe folwcytometry.Results:1.The expression of FAT10was significant inhibited by siRNA against FAT10inhepatoma carcinoma cells.2.The results of qRT-PCR and western blot show that FAT10knock down andionizing radiation is associated with up-regulation of miR-34a and Bax anddown-regulation of Bcl-2.3.We found that apoptosis rate of hepatoma carcinoma cells was significantlyenhanced after FAT10interfered or ionizing radiation. And the group ofIR+FAT10-siRNA have the highest apoptosis rate.The cell cycle analysis demonstratethat inhibiting FAT10expression induced G0/G1arrest and ionizing radiation inducedG2/M arrest. Conclusion:The expression of miR-34a and protein of Bax increased while Bcl-2reducedafter FAT10interfered,which indicated that the adiosensitivity of hepatocellularcarcinoma was enhanced after FAT10interfered.