HIF1A and non-small cell lung carcinoma: A critical aspect of NSCLC pathogenesis is the reciprocal regulation between miR-21 and the hypoxia-inducible factor HIF-1α, which drives metabolic adaptation by increasing glycolysis through HIF-1α-induced enzymes and simultaneously supporting angiogenesis via the upregulation of vascular factors such as VEGF, as shown in vitro [116,117,118].