MiR-217 Regulates Normal and Tumor Cell Fate Following Induction of Endoplasmic Reticulum Stress.

ABSTRACT: Rapidly proliferating cancer cells require a microenvironment where essential metabolic nutrients like glucose, oxygen, and growth factors become scarce as the tumor volume surpasses the established vascular capacity of the tissue. Limits in nutrient availability typically trigger growth arrest and/or apoptosis to prevent cellular expansion. However, tumor cells frequently co-opt cellular survival pathways thereby favoring cell survival under this environmental stress. The unfolded protein response (UPR) pathway is typically engaged by tumor cells to favor adaptation to stress. PERK, an endoplasmic reticulum (ER) protein kinase and UPR effector is activated in tumor cells and contributes tumor cell adaptation by limiting protein translation and balancing redox stress. PERK also induces miR

SUBMITTER: Dey N 

PROVIDER: S-EPMC10987263 | biostudies-literature | 2024 Apr

REPOSITORIES: biostudies-literature