Nicotine suppresses apoptosis by regulating α7nAChR/Prx1 axis in oral precancerous lesions
OBJECTIVE To investigate the role of nicotine on the proliferation and cell apoptosis in SCC15 oral squamous cell carcinoma cells. METHODS The growth, apoptosis, reactive oxygen species (ROS) level and nuclear factor kappalight-chain-enhancer of activated B cell (NF-κB) DNA binding activity were detected in SCC15 oral cancer cell using methly thiazolyl tetrazolium assay, flow cytometry, enzyme linked immunosorbent assay. RESULTS In SCC15 cells treated with nicotine for 48 h at different concentrations (0.1, 1, 10 µmol/L) ROS level was (98.24 ± 0.04)%, (98.50 ± 0.06)%, (98.61 ± 0.07)%, respectively, which were significantly higher than in control groups [(96.01 ± 0.58)%, P = 0.000] and the A value for cell growth was 2.19 ± 0.08, 2.20 ± 0.11 and 2.38 ± 0.08, respectively, which were significantly higher than in control groups (1.93 ± 0.13) (P < 0.05). Only 1 µmol/L nicotine induced significantly higher cell apoptosis than in other groups (P = 0.000). Cell growth was inhibited in SCC15 cells treated with 1 µmol/L nicotine for 72 h, which had statistically significant difference compared with control (P = 0.022). Cell apoptosis rate in 1 µmol/L nicotine treated groups for 24 h was significantly higher than 48 h and 72 h (P = 0.000). NF-κB expression in the nucleus were increased in SCC15 cells treated with 1 µmol/L nicotine for 24, 48 and 72 h and the A value for NF-κB DNA binding activity was 1.509, 1.093 and 0.746, respectively, which were higher than in control group (0.544). CONCLUSIONS Nicotine induced SCC15 cell growth and apoptosis, which maybe by NF-κB signal pathway activated in oral cancer cells.