[Proliferation and apoptosis of lung cancer cells regulated by gultaredoxin 3].

Objective: To investigate the effects of inhibiting glutaredoxin 3(GLRX3) expression on proliferation and apoptosis of lung cancer cells. Methods: Western blotting was used to detect the expressions of GLRX3 protein in human embryonic lung fibroblast MRC5 and lung cancer cells, including A427, A549, PC9 and H1299. GLRX3-targeted siRNA (experimental group) and negative siRNA (negative group) were transfected into A549 cells, and the cells without special treatment were blank group. The protein expression levels of GLRX3, cleaved cysteinyl aspartate specific proteinase 3(cleaved caspase-3), signal transducers and activators of transcription 3(STAT3), phosphorylated STAT3(p-STAT3) in each group at 48 hours after transfection were measured by Western blotting. The proliferation ability of differently treated cells at 24 hours, 48 hours and 72 hours after transfection were detected by CCK-8 array. The cell apoptosis at 48 hours after transfection was evaluated by flow cytometry. Results: The protein expression levels of GLRX3 in MRC5, A427, A549, PC9 and H1299 were 0.094±0.010, 0.282±0.021, 0.551±0.045, 0.423±0.039 and 0.454±0.036, respectively. The protein expressions of GLRX3 in tested lung cancer cells were significantly higher than that of MRC5 cells (all P<0.01). The GLRX3 protein expressions in blank group, negative control group and experimental group at 48 hours after transfection were 0.311±0.029, 0.328±0.032 and 0.103±0.012, respectively. GLRX3 protein expression level of experimental group in A549 cells was significantly lower than that of control group (P<0.01), whilewithout statistical difference between the negative group and blank group (P>0.05). A values of experimental group at 24, 48 and 72 hours after transfection in A549 cells were significantly different from those of blank group (all P<0.01). Percent of apoptotic cells in the experimental group was (9.52±0.56)%, which was significantly higher than that of blank group [(1.65±0.22)%] and negative control group [(1.42±0.26)%, all P<0.01]. Consistently, compared with blank group, the cleaved caspase-3 markedly increased in the experimental group (P<0.01). The protein expression of p-STAT3 in the experimental group was significantly lower than the blank group (P<0.01), while no significant difference of STAT3 protein expression was observed among all the groups (P>0.05). Conclusions: Inhibition of GLRX3 gene expression can inhibit the proliferation of lung cancer cells and induce cell apoptosis through up-regulating cleaved caspase-3 expression and down-regulating STAT3 signaling pathway.