Effects of programmde cell death 4 on growth, colony forming ability and apoptosis of bladder cancer cells

Objective To investigate the effects of programmde cell death 4 (PDCD4) on the growth, clonogenic ability and apoptosis of bladder cancer cells. Methods Lentivirus expressing PDCD4 in bladder cancer cell line T24 as overexpression group, at the same time, the cells infected with lentivirus were divided into blank group, the T24 cells without treatment were used as the control group. The levels of PDCD4 in cells were detected by real-time quantitative reverse transcriptase-polymerase chain reaction (RT-qPCR) and Western blotting. The cell growth curve was plotted by trypan blue staining, the A value of cells was detected by methyl thiazol tetrazolium (MTT), apoptosis was detected by flow cytometry, the levels of p38 mitogen activated protein kinase (p38MAPK), phosphorylation-p38MAPK (p-p38MAPK), signal transducer and activators of transcription 3 (STAT3), phosphorylation-STAT3 (p-STAT3) and cleaved cysteinyl aspartate-specific protease (Cleaved Caspase)-3 were detected by Western blotting. Results The levels of PDCD4 gene and protein in the overexpressed group were significantly higher than those in the control group (t1=12.249, P1=0.000, t2=11.601, P2=0.000) The number of cells in the overexpression group was significantly lower than that in the control group from 3 d (t1=4.075, P1=0.015, t2=6.665, P2=0.003, t3=6.340, P3=0.003). The optical density value (A value) in the over expression group was significantly lower than that in the control group, while the apoptosis rate was significantly higher in the overexpression group than in the control group (t=3.725, P=0.020). The levels of p-p38MAPK and Cleaved Caspase-3 in the overexpression group increased significantly, while the level of p-STAT3 in the cells decreased significantly (t1=10.136, P1=0.001, t2=11.867, P2=0.000, t3=6.662, P3=0.003). The levels of PDCD4, p-p38MAPK, Cleaved Caspase-3, p-STAT3, and A value, apoptosis rate in the blank group were not significantly different from those in the control group. Conclusion PDCD4 inhibits the growth of bladder cancer cells, promote cell apoptosis, reducing cell cloning ability, inhibition of phosphorylation of STAT3 in cells, promoting the phosphorylation of p38MAPK in cells, promoting the activation of Caspase-3 in cells. Key words: Programmde cell death 4; Bladder cancer; Apoptosis; Growth