Endoplasmic reticulum stress, cell death and tumor: Association between endoplasmic reticulum stress and the apoptosis pathway in tumors (Review)
Xiaojing Fu, Juanjuan Cui, Xiangjun Meng, Piyu Jiang, Qiuling Zheng, Wenwen Zhao, Xuehong Chen
Abstract
External and internal stimuli are often involved in the pathogenesis of tumors, and the deterioration of endoplasmic reticulum (ER) function within cells is also an important etiological factor of tumorigenesis resulting in the impairment of the endoplasmic reticulum, which is termed ER stress. The ER is an organelle that serves a crucial role in the process of protein synthesis and maturation, and also acts as a reservoir of calcium to maintain intracellular Ca 2+ homeostasis. ER stress has been revealed to serve a critical role in tumorigenesis. In the present review, the association between ER stress-related pathways and tumor cell apoptosis is examined. Primarily, the role of ER stress in tumor cell apoptosis is discussed, and it is stipulated that ER stress, induced by drugs both directly and indirectly, promotes tumor cell apoptosis. Contents 1. Introduction 2. UPR: A commonly defined endoplasmic reticulum stress response 3. ER stress and the tumor cell apoptosis 4. Ferroptosis and ER stress 5. Conclusion