ER Stress Signaling and its Role in Cancer Cell Death

Abstract

The endoplasmic-reticulum (ER) stress response represents a cellular process that is provoked by a number of circumstances that disturb folding of proteins in the ER. An evolutionarily conserved adaptive mechanismhas been developed by Eukaryotic cells, termed the unfolded protein response (UPR) to clear the unfolded proteins and restore ER homeostasis. The cellular functions deteriorate, in the conditions when ER stress cannot be reversed and this sometime lead to cell death. The poor vascularization, low oxygen supply, nutrient deprivation, and acidic pH in the tumor microenvironment stimulate the ER stress. UPR has been shown to exert a significantcytoprotective part in speedily growing cancers as it helps folding of newly synthesized proteins required for the growth of the tumor.Accumulating evidence showed that ER stress-induced cellular dysfunction and cell death are the major contributors to many diseases and making the modulators of ER stress pathways potentially attractive targets for therapeutics discovery. Herein, we will briefly summarize gesticulating cascade activated upon ER stress and its role in cancer cell death.