School of Basic Medicine, Qingdao University, Qingdao, Shandong 266071, P.R. China.
Qingdao Municipal Hospital, Qingdao (Group), Qingdao, Shandong 266071, P.R. China.
Oncol Rep. 2021 Mar;45(3):801-808. doi: 10.3892/or.2021.7933. Epub 2021 Jan 12.
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 Ca2+ 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.
外部和内部刺激通常与肿瘤的发病机制有关，细胞内内质网（ER）功能的恶化也是导致内质网损伤的肿瘤发生的重要病因，这种内质网损伤被称为内质网应激。ER 是一种在蛋白质合成和成熟过程中起关键作用的细胞器，也是钙的储存库，以维持细胞内 Ca2+的动态平衡。内质网应激已被揭示在肿瘤发生中起关键作用。在本综述中，检查了与 ER 应激相关途径和肿瘤细胞凋亡之间的关联。首先，讨论了 ER 应激在肿瘤细胞凋亡中的作用，并规定了药物直接和间接诱导的 ER 应激促进肿瘤细胞凋亡。
