Effect of Radiotherapy on Cisplatin-Resistant Ovarian Cancer Cells
Objective To explore the effect of radiotherapy on the drug resistance of ovarian cancer cisplatin(CDDP)resistant cells and explore the related mechanisms.Methods SKOV3 cell line and SKOV3/CDDP-resistant cell line of logarithmic stage ovarian cancer were taken.Dimethylthiazole(MTT)method was used to detect the sensitivity of SKOV3,SKOV3/CDDP to CDDP and the killing effect of radiotherapy on SKOV3/CDDP.The log-phase SKOV3/CDDP-resistant cell line was taken and intervened with 0.5 Gy×4 low-dose split radiotherapy,which was set up as the low-dose split radiothera-py group,and the untreated SKOV3/CDDP-resistant cell line was taken as the blank group,and the plate cloning assay was performed to determine the clone-forming ability of the two groups.Flow cytome-try was used to determine the apoptosis rate,propidium iodide(PI)staining was used to determine the cell cycle,and Western blot was used to detect cyclin-D1,cellular-myeloma virus oncogene(c-myc),β-catenin and p-β-catenin protein expression.Results The half inhibitory concentration(IC50)of CDDP on SKOV3 and SKOV3/CDDP cells was 2.41 and 6.15 mg·L-1,respectively,and the resistance index(RI)of SKOV3/CDDP to CDDP was 2.55 times.The IC50 of CDDP on SKOV3/CDDP cells was 6.15,5.17,3.92 and 4.31 mg·L-1 at no radiotherapy,0.5 Gy,0.5 Gy×4 times and 2 Gy,respectively;and the reversal fold(RFT)of resistance was 1.19 times,1.57 times,and 1.43 times at 0.5 Gy,0.5 Gy×4 times,and 2 Gy,respectively.The clone formation rate,the proportion of S,G2/M,the relative expres-sion of cyclin-D1 and c-myc protein,p-β-catenin/β-catenin in the low-dose fractional radiotherapy group were lower than those of the blank group,of which the apoptosis rate,the proportion of G0/G1 were higher than those of the blank group(P<0.05).Conclusion Low-dose fractional radiotherapy can inhibit the proliferation of CDDP-resistant ovarian cancer cells,promote their apoptosis,and have chemosensitizing effects,which is presumably related to the inhibition of Wnt/β-catenin signaling pathway.