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. 2020 Mar 20;7(1-2):14–16. doi: 10.18632/oncoscience.498

Figure 1. Chronic MET inhibition facilitates metabolic reprogramming to drive fatty acid oxidation.

Figure 1

The receptor kinase c-MET can be inhibited by crizotinib. Chronic c-MET inhibition results in paradoxical reactivation of ERK followed by CREB and PGC1α upregulation. In addition, there is an enhancement of fatty acid oxidation (FAO) coupled with up-regulation of genes involved in FAO (ACADVL, ACADSB, CPT2, FABP3). Likely, increased anaplerosis contributes to proper running of the tricarboxylic acid cycle. Related to this phenotype, there is activation of OXPHOS (oxidative phosphorylation) and enhanced mitochondrial abundance.