Dihydroartemisinin, a potential PTGS1 inhibitor, potentiated cisplatin-induced cell death in non-small cell lung cancer through activating ROS-mediated multiple signaling pathways - Ni, Lianli; Zhu, Xinping; Zhao, Qi; Shen, Yiwei; Tao, Lu; Zhang, Ji; Lin, Han; Zhuge, Weishan; Cho, Young-Chang; Cui, Ri; Zhu, Wangyu (Neoplasia (New York, N.Y.), 2024)
Keywords: Apoptosis; Artemisinins - pharmacology; Artemisinins - therapeutic use; Carcinoma, Non-Small-Cell Lung - drug therapy; Carcinoma, Non-Small-Cell Lung - genetics; Carcinoma, Non-Small-Cell Lung - metabolism; Cell Death; Cell Line, Tumor; Cisplatin; Cisplatin - pharmacology; Cyclooxygenase 1 - metabolism; Cyclooxygenase Inhibitors - pharmacology; Dihydroartemisinin (DHA); Endoplasmic reticulum (ER) stress; Humans; Lung Neoplasms - pathology; Mitogen-activated protein kinases (MAPK); Original Research; p38 Mitogen-Activated Protein Kinases - metabolism; Prostaglandin G/H synthase 1 (PTGS1); Reactive oxygen species (ROS); Reactive Oxygen Species - metabolism; Signal Transduction; BC; NO; DMSO; JNK; ALT; MDA; MTT; PTGS2; MPO; BP; PTGS1; Dihydroartemisinin (DHA); MF; EC; Prostaglandin G/H synthase 1 (PTGS1); CC; PBS; Mitogen-activated protein kinases (MAPK); AST; Endoplasmic reticulum (ER) stress; NSCLC; CI; H&E; Reactive oxygen species (ROS); GO; COX; ER; Cisplatin; LAC; eIF2α; DCFH-DA; NAC; TSV; ROS; DHA; ATF4; DC