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- TIPRL potentiates survival of lung cancer by inducing autophagy through the eIF2α-ATF4 pathway
- Su Jin Jeon; Jun Ho Ahn; D Halder; Hyun Soo Cho; Jung Hwa Lim; Soo Young Jun; Jeong Ju Lee; Ji Yong Yoon; Min Hyuk Choi; Cho Rok Jung; J M Kim; Nam-Soon Kim
- Bibliographic Citation
- Cell Death & Disease, vol. 10, no. 12, pp. 959-959
- Publication Year
- 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 the eIF2α-ATF4 pathway, thereby inducing autophagy. Conversely, TIPRL depletion increased apoptosis by reducing autophagic clearance, which was markedly enhanced in TIPRL-depleted A549 xenografts treated with 2-deoxy-D-glucose. Overall, the study indicated that TIPRL is a potential regulator of autophagy and an important drug target for lung cancer therapy.
- Springer-Nature Pub Group
- Appears in Collections:
- Division of Research on National Challenges > Stem Cell Convergenece Research Center > 1. Journal Articles
Division of Biomedical Research > Rare Disease Research Center > 1. Journal Articles
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