Effect of NLRC3 expression knock-down on growth of normal human bronchial epithelial BEAS-2B cells

AIM To investigate the effect of NOD-like receptor family caspase recruitment domain containing 3 (NLRC3) expression knock-down on the viability and apoptosis of normal human bronchial epithelial BEAS-2B cells and its mechanism. METHODS The small interfering RNA (siRNA) fragments of NLRC3 gene were transfected into BEAS-2B cells using Lipofectamine 2000 transfection reagent to knock down the NLRC3 expression. The interference fragment was screened by RT-qPCR. The cell viability was measured by MTT assay. The mitochondrial membrane potential was detected by JC-1 staining. The apoptotic rate was analyzed by flow cytometry with annexin V-FITC/PI staining. The protein expression levels of Bcl-2 and Bax were determined by Western blot. RESULTS The interference segment 3 of NLRC3 gene (siNLRC3-3) displayed the best interference effect on NLRC3 expression in BEAS-2B cells (P<0.01). Knock-down of NLRC3 expression in BEAS-2B cells enhanced the cell viability (P<0.01). Knock-down of NLRC3 increased the mitochondrial membrane potential, and decreased the apoptotic rate (P<0.05). Moreover, knock-down of NLRC3 significantly up-regulated Bcl-2 protein expression and significantly down-regulated Bax protein expression (P<0.01). CONCLUSION Knock-down of NLRC3 expression enhances the viability and inhibits the apoptosis of BEAS-2B cells, which may be related to increase in the expression of Bcl-2 protein and decrease in the expression of Bax protein.