Research On Effection And Mechanism Of Radiosensitivity Of Non-small Cell Lung Cancer Cell Line H358 Following Gefitinib Treatment

Objective: To observe whether gefitinib can radiosentisize NSCLC H358 cell line and investigate the mechanism by which gefitinib, a selective EGFR tyrosine kinase inhibitor, restores the radiosensitivity of NSCLC cells.Methods: NSCLC cell line H358 was divided into X ray group and Gefitinib interfering group. The former was irradiated with X ray only and the latter was treated with 1 umol/L gefitinib for 24 h before irradiation at the same conditions. Then, they were tested for clonogenic cell survival assay, forγ-H2AX repair and EGFR foci using immunostaining for confocal microscopy and for nuclear EGFR expression using western blotting.Results: In clonogenic cell survival assay, the survival fraction in Gefitinib interfering group was lower than X ray group at different does. SF2 of them were 0.000865 and 0.0111. SER was 2.815. Immunostaining for confocal microscopy suggested that the number of nuclearγ-H2AX foci in Gefitinib interfering group is bigger than that in X ray group. The nuclearγ-H2AX foci also stayed longer in the former group. Nearly all EGFR tanslocated into nucleus within 1 h in X ray group, but it stayed in cytoplasma all the time in Gefitinib interfering group tested for immunostaining for confocal microscopy and western blotting. Western blotting was tested for SPSS13.0, p=0.042.Conclusion: Gefitinib, at cell levels, radiosensitizes EGFRwt NSCLC H358 through blockading EGFR nulear translocation as one of its mechanisms.