Abstract: Objective To investigate the role and possible mechanism of LRIG1 in SKOV3, siRNALRIG1 KOV3, KOV3/VP16 and siRNALRIG1 KOV3/VP16. Methods The cell proliferation of SKOV3, siRNALRIG1 KOV3, KOV3/VP16 and siRNALRIG1 KOV3/VP16 were detected by MMT at different concentrations of VP16, which had been con-cultured for 48 hours. Cell proliferation was detected by plate cloning. Cell apoptosis was detected by flow cytometry. LRIG1 gene expression was detected by quantitative real-time PCR. Results IC50 of SKOV3, siRNALRIG1 KOV3, KOV3/VP16 and siRNALRIG1 KOV3/VP1 were 62.90 μg/L, 115.49 μg/L, 156.50 μg/L and 195.42 μg/L, respectively, with the drug resistance index of 1.8, 2.5 and 3.1 respectively. Compared with SKOV3, the cloning rates had increased (the mean differences were 8.000, 37.692 and 72.000, P < 0.05), the LRIG1 mRNA (the mean differences were 2.994, 88.366 and 279.004, P < 0.05) and apoptotic cells (the mean difference were 48.942, 63.485 83.659, P < 0.05) had decreased significantly in siRNALRIG1 KOV3, SKOV3/VP16 and siRNALRIG1 KOV3/VP16 cells. Compared with siRNALRIG1 KOV3, the cloning rates had increased (the mean differences were 25.000 and 58.824, P < 0.05), the LRIG1 mRNA (the mean differences were 47.478 and 180.147, P < 0.05) and apoptotic cells (the mean differences were 53.678 and 42.687, P < 0.05) had decreased in SKOV3/VP16 and siRNALRIG1 KOV3/VP16 cells (P < 0.05). Compared with SKOV3/VP16, the cloning rates had increased (the mean difference was 10.000, P < 0.05), the LRIG1 mRNA (the mean difference was 92.784, P < 0.05) and apoptotic cells (the mean difference was 37.625, P < 0.05) had decreased in siRNA LRIG1 KOV3/VP16 cells (P < 0.05). Conclusions The LRIG1 gene can affect drug sensitivity of SKOV3 for lower LRIG1 could decrease the apoptosis of cells.