Human Leptin Triggers Proliferation of A549 Cells Via Blocking ER Stress Related Apoptosis
Lung cancer is a disease characterized by uncontrolled cell growth in tissues of the lung. Leptin is a pleiotropic hor-mone with antiapoptotic and proliferative role involved in several systems. However, there is still no knowledge about the antiapoptotic mechanism of leptin in non-small cell lung cancer (NSCLC). So, the antiapoptotic mechanism of leptin was investigated in NSCLC. The proliferation, apoptosis, and the specific mechanism of leptin transfected cells were analyzed in this study. Leptin, p-Perk, IRE1, cleaved ATF6, spliced XBP1, eIF2-б, TRAF2, CHOP, and caspase-12 protein were detected by western blot, and the endoplasmic reticulum (ER) stress-related mRNA were detected by semi-reverse transcription PCR (RT-PCR). Leptin in A549 and transfected cells could inhibit the cisplatin-activated ER stress-associated mRNA transcription and activation of proteins. ER stress unfolded protein response (UPR) proteins, PERK and ATF6, were involved in leptin-triggered apoptosis. XBP1 and TRAF2 were increased significantly when treated with cisplatin in A549#siLPT and non-transfected cells. CHOP expression was blocked in A549 and transfected cells (LPT-PeP and LPT-EX cells). In conclusion, leptin can promote the proliferation of A549 cells through blocking the ER stress-mediated apoptosis. This blocking is mediated by p-Perk and the ATF6 pathway through blocking of CHOP activation.