Effect of nicotine on the proliferation and cell apoptosis of oral squamous cell carcinoma SCC15 cells / 中华口腔医学杂志

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the role of nicotine on the proliferation and cell apoptosis in SCC15 oral squamous cell carcinoma cells.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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).</p><p><b>CONCLUSIONS</b>Nicotine induced SCC15 cell growth and apoptosis, which maybe by NF-κB signal pathway activated in oral cancer cells.</p>