Fig. 3: Effects of CPT1C silencing in cancer cell metabolism.
From: To be or not to be a fat burner, that is the question for cpt1c in cancer cells
Downregulation of CPT1C favors cancer cell senescence, as demonstrated by the increased b-galactosidase marker, diminished telomere length, cell cycle arrest, and activation of the senescence-associated secretory phenotype. CPT1C downregulation, as revealed by lipidomic analysis, results in great lipid remodeling, including impaired expression of lipid metabolic genes, decreased cardiolipin levels, diminished phosphatidylcholine/phosphatidylethanolamine (PC/PE) ratio, increased levels of FAs, triacylglycerol, and sphingolipids, and lipid droplet accumulation. CPT1C downregulation impairs mitochondrial morphology, function (decreased mitochondrial respiration, decreased FAO, and altered electrochemical gradient) and biogenesis. All those changes result in decreased ATP levels and oxidative stress.
