Effects of LEF1 and CTNNB1 on cycle arrest, apoptosis and radiation resistance of esophageal carcinoma cells / 中华放射肿瘤学杂志

ABSTRACT

Objective:To investigate the relationship between the expression level of lymphocyte enhancer-binding factor 1(LEF1) and CTNNB1 and the cycle arrest, apoptosis and radiation resistance of esophageal cancer cells and unravel the related mechanisms.Methods:Recombinantplasmids and empty plasmids expressing LEF1 and CTNNB1were constructed and transfected into esophageal cancer cells. RT-PCR assay was used to detect the transfection efficiency of the plasmids. Clone formation assay, CCK8 assay, cell cycle test by flow cytometry, apoptosis test by flow cytometry and Western blot were performed to detect the differences in theradioresistance, proliferation, cell cycle and apoptosis of esophageal cancer cells before and after transfection.Results:The survival rate of clonal colony cells in the pGEX-LEF1+ pCMV6-CTNNB1 group was significantly better than those in other groups ( P<0.05). The proliferation of clonal colony cellsat 72 h, 96 h and 120 h in the pGEX-LEF1+ pCMV6-CTNNB1 group was significantly better than those in the pGEX+ pCMV6, pGEX-LEF1+ pCMV6 and pCMV6-CTNNB1+ pGEX groups (all P<0.05). The percentage of G 2 phase arrest cells in the pGEX-LEF1+ pCMV6-CTNNB1 group was significantly higher than those in the other groups (all P<0.05). The apoptosis rate of esophageal cancer cells in the pGEX-LEF1+ pCMV6-CTNNB1 group was significantly lower compared with those in the pGEX+ pCMV6, pGEX-LEF1+ pCMV6 and pCMV6-CTNNB1+ pGEX groups (all P<0.05). The expression levels of Bax and Caspase 3 proteins in the pGEX-LEF1+ pCMV6-CTNNB1 group were significantly lower than those in the pGEX+ pCMV6, pGEX-LEF1+ pCMV6 and pCMV6-CTNNB1+ pGEX groups (all P<0.05). The expression level of Bcl-2 protein in the pGEX-LEF1+ pCMV6-CTNNB1 group was significantly higher compared with those in the other groups (all P<0.05). Conclusion:LEF1 and CTNNB1 can regulate the proliferation and G 2 phase arrest of esophageal cancer cells after radiation intervention by mediating the Wnt signaling pathway, and improve the radiation resistance of esophageal cancer cells by inhibiting cell apoptosis.