Objective:To investigate the effect of elevated retinoic acid inducible gene-I (RIG-I)on the growth of NIT-1 pancreatic β-cell and possible mechanisms during this process. Methods:Different concentrations of retinoic acid (RA)were used to activate RIG-I with different periods. Cell viability was assessed by MTT colorimetric assay. RIG-I was detected using real-time RT-PCR and Western blot analysis. Cell cycle distribution was measured by FACS analysis,and cell cycle protein p27 was further detected by Western blot analysis. Results:Retinoic acid upregulated the mRNA and protein level of RIG-I in NIT-1 cells (P < 0.05). Elevated RIG-I significantly inhibited the viability of NIT-1 cells in a dose-dependent manner (P < 0.05). Furthermore,elevated RIG-I induced an increase in the proportion of cells at the G1 phase and a corresponding decrease in the number of cells at the S phase (P < 0.05). Additionally,elevated RIG-I caused a significant increase of p27 protein (P < 0.05). Conclusion:The results suggest that activated RIG-I induced upregulation of p27 in pancreatic β-cell,which inhibits proliferation through cell cycle arrest at the G1 phase,and ultimately results in an overall β-cell mass deficiency.