Fig 1: A schematic model of metabolic mechanisms in gefitinib-resistant Ire cells. A proposed model of the metabolic reprogramming that occurs during the development of TKI-resistant non-small cell lung cancer (NSCLC). In gefitinib-resistant NSCLC, EGFR translocated to mitochondria and strengthens mitochondrial oxidative phosphorylation (OXPHOS) capacity and complexes’ activity. Concomitantly, MCT-1, LDHB, and PDHA1 were highly expressed in gefitinib-resistant NSCLC. The inhibition of MCT-1 by AZD3965 reduced cell proliferation and cell motility in gefitinib-resistant NSCLC. Abbreviations: EGF, epidermal growth factor; EGFR, epidermal growth factor receptor; MCT, monocarboxylate transporter; LDH, lactate dehydrogenase; PDH, pyruvate dehydrogenase; PDK, pyruvate dehydrogenase kinase; C, complex; TCA cycle, tricarboxylic acid cycle; OXPHOS, oxidative phosphorylation.