Sodium selenite influence the proliferation and apoptosis of lung cancer cell A549 by promoting the phosphorylation of p38 mitogen activated protein kinase

Objective To study the influence of sodium selenite (Na2SeO3) on the proliferation, apoptosis and p38 Mitogen activated protein kinase signaling pathway of of lung cancer cell A549. Methods Lung cancer cell A549 were treated with Na2SeO3 by the final concentration of 0.0, 2.5, 5.0, 10.0 μmol/L respectively. The effect of Na2SeO3 on the proliferation lung cancer cell A549 was measured by methyl thiazol tetrazolium (MTT) after cultured 24, 48, 72 h. The effect of Na2SeO3 on the apoptosis of lung cancer cell A549 were ananlyzed with flow cytometry after cultured 48 h. The effect of Na2SeO3 on the expression of apoptosis related protein B cell lymphoma/leukemia-2 (bcl-2), Caspase-3 and p38 mitogen activated protein kinase (p38MAPK) signaling pathway protein p38MAPK and phosphorylated p38MAPK (p-p38MAPK) in lung cancer cell A549 were detected by Western blotting. Results Na2SeO3 can inhibit the proliferation of Lung cancer cell A549, also has a dose dependent and time dependent, the difference is very significant compared with the control group. Lung cancer cell A549 were treated with a concentration of 2.5, 5.0 and 10.0 μmol/L of Na2SeO3 after cultured 48 h, Observed that with the increase of Na2SeO3 concentration, apoptosis rate increased, bcl-2 protein expression gradually down regulated, Caspase-3 and p-p38MAPK protein expression gradually increased (Caspase-3: t2.5 μmol/L=6.524, P2.5 μmol/L=0.006; t5.0 μmol/L=8.283, P5.0 μmol/L=0.003; t10.0 μmol/L=9.345, P10.0 μmol/L=0.002; p-p38MAPK: t2.5 μmol/L=7.173, P2.5 μmol/L=0.005; t5.0 μmol/L=8.687, P5.0 μmol/L=0.003; t10.0 μmol/L=9.754, P10.0 μmol/L=0.001), the difference was very significant compared with the control group. However, the expression of p38MAPK protein in different concentrations of Na2SeO3 treatment group had no significantly difference, compared with the control group, there was no significant difference, yet (t2.5 μmol/L=1.325, P2.5 μmol/L=0.283; t5.0 μmol/L=1.364, P5.0 μmol/L=0.298; t10.0 μmol/L=1.321, P10.0 μmol/L=0.289). Conclusion Na2SeO3 can inhibit the proliferation and promote the apoptosis of lung cancer cells A549, the possible molecular mechanism is to promote the phosphorylation of p38MAPK. Key words: Na2SeO3; Lung cancer cells A549; p38 mitogen activated protein kinase; Cell proliferation; Cell apoptosis