Fig. 3

Mitochondrial metabolic and stress adaptations in cancer. Cancer cells develop sophisticated metabolic strategies to sustain proliferation under challenging conditions. These adaptations include increased glucose uptake (Warburg effect), increased glutamine metabolism to replenish energy cycles, the activation of one-carbon metabolism for biosynthesis, and mitochondrial reprogramming to support lipid production and redox balance. By dynamically adjusting metabolic pathways, cancer cells can generate essential metabolic intermediates, maintain bioenergetic efficiency, and survive in nutrient-poor or hypoxic environments that typically inhibit cellular growth and function. 3-PG 3-phosphoglycerate, 5mTHF 5-methyltetrahydrofolate, AMP adenosine monophosphate, ATP adenosine triphosphate, CH2-THF 5,10-methylene tetrahydrofolate, GLUL glutamine synthetase, G6P glucose-6-phosphate, HIF-1α hypoxia-inducible factor 1-alpha, MET methionine, mTORC1 mechanistic target of rapamycin complex 1, mLST8 mammalian lethal with SEC13 protein 8, MYC MYC Proto-Oncogene, NADPH nicotinamide adenine dinucleotide phosphate, OXPHOS oxidative phosphorylation, PI3K phosphatidylinositol 3-kinase, ROS reactive oxygen species, SAH S-adenosyl homocysteine, SAM S-adenosyl methionine, SLC1A5 solute carrier family 1 member 5, SLC7A5 solute carrier family 7 member 5, SREBP sterol regulatory element-binding protein, TCA cycle tricarboxylic acid cycle, THF tetrahydrofolate, VDAC voltage-dependent anion channel, α-KG alpha-ketoglutarate. This figure was created with BioRender (https://biorender.com/)