Programmed cell death 4 enhances radiosensitivity of pancreatic cancer cells

Objective To investigate the effect and mechanism of programmed cell death 4 ( PDCD4 ) on radiosensitivity of pancreatic cancer cells. Methods Pancreatic cancer tissues and corresponding adjacent tissues were collected, the expression level of PDCD4 was detected by RT-PCR and Western blot. Human pancreatic cancer cells Sw1990 were transfected with PDCD4 overexpression vector ( group pIRES2-PDCD4 ) , empty vector ( pIRES2 group ) , and treated with transfection reagent, respectively. The expression level of PDCD4 was detected by RT-PCR and Western blot. After radiation treatment, cell apoptosis was detected by flow cytometry, cell survival was detected by clone assay, and the expression levels ofβ-catenin, c-myc and Cleaved Caspase-3 were detected by Western blot. Results The expression of PDCD4 mRNA and protein in pancreatic cancer tissues was significantly lower than that in adjacent tissues (t=4. 869, 9. 208, P<0. 05). The expression of PDCD4 mRNA and protein in pIRES2-PDCD4 group was significantly lower than that in the non-transfection group ( t =9. 074, 18. 927, P <0. 05). After radiation, the apoptosis rate and Cleaved Caspase-3 level in the pIRES2-PDCD4 group were significantly higher than those in the non-transfection group (t =3. 670, 4. 086, P <0. 05), while the expression levels of β-catenin and c-myc in the cells were significantly lower than those in the non-transfection group (t =9. 242, 17. 644, P <0. 05). The radiosensitivity of pIRES2-PDCD4 group was higher than that of non-transfection group, and the sensitization ratio was 1. 843. Conclusions PDCD4 can increase radiosensitivity and promote apoptosis of pancreatic cancer cells, to which the Wnt signaling pathway may be related.