Tumorigenic and Immunosuppressive Effects of Endoplasmic Reticulum Stress in Cancer

Abstract

SUMMARY Malignant cells utilize diverse strategies that enable them to thrive under adverse conditions while simultaneously inhibiting the development of anti-tumor immune responses. Hostile microenvironmental conditions within tumor masses, such as nutrient deprivation, oxygen limitation, high metabolic demand and oxidative stress disturb the protein folding capacity of the Endoplasmic Reticulum (ER), thereby provoking a cellular state of “ER stress”. Sustained activation of ER stress sensors endows malignant cells with greater tumorigenic, metastatic and drug resistant capacity. Additionally, recent studies have uncovered that ER stress responses further impede the development of protective anti-cancer immunity by manipulating the function of myeloid cells in the tumor microenvironment. Here, we discuss the tumorigenic and immunoregulatory effects of ER stress in cancer, and we explore the concept of targeting ER stress responses to enhance the efficacy of standard chemotherapies and evolving cancer immunotherapies in the clinic.

Whole-Transcriptome Analysis of CD133+CD144+ Cancer Stem Cells Derived from Human Laryngeal Squamous Cell Carcinoma Cells

“…Previous studies have suggested the endoplasmic reticulum stress could determine apoptosis and cell death in cancers [37,38]. SSR1, regulated by miR-4521, was associated with the pathway of protein processing.…”

Canopy Homolog 2 Expression Predicts Poor Prognosis in Hepatocellular Carcinoma with Tumor Hemorrhage

“…It is known that during TH, red blood cells and platelets aggregate around tumor cells, facilitating the formation of cancer cell nests and providing protection against immune responses and shear stress [5][6][7]. TH has been demonstrated to be a poor prognostic factor for patients with HCC [8].…”

Transcriptomic Profiling of MDA-MB-231 Cells Exposed to Boswellia Serrata and 3-O-Acetyl-Β-Boswellic Acid; ER/UPR Mediated Programmed Cell Death

“…Yet at the same time, activation of main pathways in the ER/UPR an also trigger programmed cell death (PCD) evidenced by many natural anti-cancer agents (31-41) alkylating/ platinum based drugs and anti-cancer steroids (42)(43)(44)(45)(46)(47) further understanding of the pro-survival/pro-death ER/UPR processes and the relevance timing on cancer initiation, progression and treatment (48). It is believed that if we can further understand control of ER stress regulators on cancer growth, we can successfully use this information to overcome acquired resistance to (49) and augment existing (50). The data from this study show BSE and 3-OAβBA to impact several processes within the ER/UPR.…”