Effects of HBXIP protein expression on the proliferation and radiosensitivity of cervical cancer cells

Objective To explore t he effects of (hepatitis B X-interacting protein) HBXIP down-regulation on the proliferation and radiosensitivity of cervical cancer ME-180 cells. Method According to the different treatment methods, cervical cancer ME-180 cells were divided into different groups: (1)The cervical cancer ME-180 cells were divided into 4 groups: control group, 4 Gy γ ray irradiation group, HBXIP-siRNA transfection group and HBXIP-siRNA transfection+γ ray irradiation group. cervical cancer ME-180 cell proliferation was detected by MTT and clonogenic assays. The expression of Bcl-2 and Bid mRNA was detected by quantitative real-time polymerase chain reaction, and the phosphorylation of AKT protein was measured by Western blot analysis. (2)The cervical cancer ME-180 cells were divided into 3 groups: control group, HBXIP-siRNA transfection group and HBXIP-siRNA+AKT transfection group. Then the three groups of cells were irradiated with different doses of γ ray, and the cervical cancer ME-180 cell proliferation was detected by clonogenic assay. Statistical significance of the results was determined by SPSS statistical software and analyzed by Student t-test. P<0.05 were considered statistically significant. Results MTT and clonogenic assays showed that, compared with the cells irradiated alone, the cervical cancer ME-180 cells irradiated in the presence of HBXIP-siRNA had significantly decreased proliferation (t=11.63, 12.17, P<0.01). The decreased proliferation was accompanied by a decreased expression of Bcl-2 protein (t=10.88, P<0.01) and an increased expression of Bid protein (t=9.31, P<0.01). The transfection with HBXIP-siRNA inhibited the increased HBXIP protein expression and AKT phosphorylation, which were caused by radiation. The enhanced AKT expression significantly reduced the HBXIP-siRNA inhibition of cervical cancer ME-180 cell proliferation after irradiation as compared with that of the HBXIP-siRNA alone (t=8.96, P<0.01). Conclusion HBXIP down-regulation reduced the proliferation and increased the radiosensitivity of cervical cancer ME-180 cells by mediating AKT activation. Key words: HBXIP; RNA, small interfering; Uterine cervical neoplasms; Cell proliferation; Radiation tolerance