Study On The Molecular Mechanism Of Apoptosis Of Lung Cancer Cells Induced By Stattic Combined With LCS-1

Objective:To observe the effects of Stattic an d LCS-1 on the apoptosis of lung cancer cells H446,PC-9,H1299,A549 and to explore its mechanism.To observe the effect of the combination of the two on apoptosis of lung cancer cells.Methods:1.Detection of cell apoptosis by flow cytometry.2.Detection of phosphorylated Stat3 expression by Western-Blot.3.Detection of GSH level in cells by DTNB-GSSG recycling.4.Detection of ROS expression in cells by DCF staining.5.Detection of m RNA expression of SOD1,SOD2 and SOD3 in cells by RT-PCR.Results:1.Stattic induces cell apoptosis in lung cancer cells.2.Stattic-induced cell apoptosis is STAT3-independent.3.Stattic induced the depletion of GSH and the induction of ROS.4.ROS scavengers reverse Stattic-induces cell apoptosis in lung cancer cells.5.The levels of cell apoptosis induced by Stattic is related to the expression of SOD1.6.LCS-1 induces cell apoptosis in lung cancer cell.7.LCS-1-induced cell apoptosis is ROS-dependent.8.Stattic synergizes with LCS-1 to induce cell apoptosis in lung cancer cells.9.Stattic synergized with LCS-1 to induce ROS production contributing to cell apoptosis.Conclusion:1.Stattic induced oxidative stress-dependent lung cancer cell apoptosis by consuming GSH and inducing ROS instead of stat3-dependent lung cancer cell apoptosis Stattic induces STAT3-independent cell death in lung cancer cells.2.Stattic induced apoptosis of lung cancer cells by synergistically upregulation of ROS by Stattic through consumption of LCS-1.