ANNOUNCEMENTS
Non-small cell lung cancer (NSCLC) leads to the highest cancer-related mortality worldwide. When tumor cells undergo a hypoxic condition that is characterized by low oxygen levels faced by the cancer cells, it triggers a metabolic switch from oxidative phosphorylation towards aerobic glycolysis, a phenomenon known as the Warburg effect. This metabolic shift promotes angiogenesis, tumor progression and immune evasion. The cGAS (cyclic GMP-AMP synthase)-STING(Stimulator of interferon genes) pathway is an innate immunity mechanism which gets activated when it detects cytosolic DNA. TREX1(Three prime repair Exonuclease 1) is an enzyme that degrades cytosolic DNA, suppressing immune activation. In this study, Hypoxia was induced using 100μM concentration of Cobalt Chloride(CoCl₂) in NCI-H23(National Cancer Institute -Human 23) lung Adenocarcinoma cells. Trypan Blue viability Assay confirmed minimal cell death. qPCR analysis showed the increase in expression levels of TREX1, VEGFA, HK1 and PKM2, and downregulation of cGAS levels under hypoxia. These findings suggest that hypoxia- induced metabolic plasticity promotes immune suppression by upregulating TREX1, highlighting TREX1 as a potential biomarker and therapeutic target in NSCLC.
Keywords: Hypoxia, Metabolic plasticity, TREX1, cGAS-STING, Non-small cell lung cancer.
