simultaneous induction of non-canonical autophagy and apoptosis in cancer cells by ros-dependent erk and jnk activation同时感应非规范自噬和凋亡的肿瘤细胞通过ros-dependent erk和物激活.pdfVIP

Simultaneous Induction of Non-Canonical Autophagy and Apoptosis in Cancer Cells by ROS-Dependent ERK and JNK Activation 1,2. 1. 1 1 3 Chew Hooi Wong , Kartini Bte Iskandar , Sanjiv Kumar Yadav , Jayshree L. Hirpara , Thomas Loh , Shazib Pervaiz1,2,4,5* 1 Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore, 2 NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore, Singapore, 3 Department of Otorhinolaryngology, National University Hospital System, Singapore, Singapore, 4 Cancer and Stem Cell Biology Program, Duke-NUS Graduate Medical School, Singapore, Singapore, 5 Singapore-MIT Alliance, Singapore, Singapore Abstract Background: Chemotherapy-induced reduction in tumor load is a function of apoptotic cell death, orchestrated by intracellular caspases. However, the effectiveness of these therapies is compromised by mutations affecting specific genes, controlling and/or regulating apoptotic signaling. Therefore, it is desirable to identify novel pathways of cell death, which could function in tandem with or in the absence of efficient apoptotic machinery. In this regard, recent evidence supports the existence of a novel cell death pathway termed autophagy, which is activated upon growth factor deprivation or exposure to genotoxic compounds. The functional relevance of this pathway in terms of its ability to serve as a stress response or a truly death effector mechanism is still in question; however, reports indicate that autophagy is a specialized form of cell death under certain conditions. Methodology/Principal Findings: We re