TIPRL potentiates survival of lung cancer by inducing autophagy through the eIF2α-ATF4 pathway.

ABSTRACT: Autophagy, an intracellular system of degrading damaged organelles and misfolded proteins, is essential for cancer cell survival. Despite the progress made towards understanding the mechanism, identification of novel autophagy regulators presents a major obstacle in developing anticancer therapies. Here, we examine the association between the TOR signaling pathway regulator-like (TIPRL) protein and autophagy in malignant transformation of tumors. We show that TIPRL upregulation in non-small cell lung cancer (NSCLC) potentiated autophagy activity and enabled autophagic clearance of metabolic and cellular stress, conferring a survival advantage to cancer cells. Importantly, the interaction of TIPRL with eukaryotic initiation factor 2α (eIF2α) led to eIF2α phosphorylation and activation of th

SUBMITTER: Jeon SJ 

PROVIDER: S-EPMC6925247 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature