USP11介导肝细胞癌细胞辐射抵抗的初步研究

Objective: To investigate the role of USP11 in the regulation of radiosensitivity of hepatocellular carcinoma (HCC) cells. Methods: The corresponding cell models were constructed by overexpressing or silencing USP11 in human HCC cell lines Huh7 and HepG2; clonal formation assay was used to detect the effect of USP11 on the radiosensitivity of Huh7 and HepG2 cells; flow cytometry was utilized for detecting the influePreliminary study on USP11-mediated radioresistance of hepatocellular carcinoma cellsnce of USP11 on apoptosis level of irradiated HCC cells; Immunofluorescence were utilized for detecting the changes of DNA damage related protein γ-H2AX expression. Results: Overexpression of USP11 can increase the clonal formation of Huh7 and HepG2 cells, suggesting that USP11 can promote the radiation resistance of HCC cells; silencing USP11 can inhibit the clonal formation of Huh7 and HepG2 cells, increase the level of cell apoptosis, and increase the expression of γ-H2AX protein after ionizing radiation, suggesting that targeted inhibition of USP11 can enhance the radiosensitivity of HCC. Conclusions: USP11 is a key regulator of radiosensitivity in HCC and a potential new target for radiosensitization. Its mechanism of action may be related to the regulation of radiation-induced apoptosis and DNA damage in HCC cells, but the specific molecular regulatory mechanisms involved still need to be further investigated.