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. 2022 Sep 24;13(9):817. doi: 10.1038/s41419-022-05259-w

Fig. 1. Mutant KRAS mediated metabolic alterations.

Fig. 1

The active oncogenic KRAS mutant triggers glycolysis for energy generation and building block biosynthesis and shunting into the nonoxidative arm of the pentose phosphate pathway for nucleic acid biosynthesis and the hexosamine biosynthesis pathway for UDP-N-acetylglucosamine biosynthesis through upregulation of key enzymes in glycolysis. In addition, micropinocytosis and autophagy ensure that mutant KRAS cancer cells obtain energy and biosynthetic building blocks from the microenvironment. GLUT1 glucose transporter 1, HK1/2 hexokinases 1 and 2, PFK1 phosphofructokinase 1, LDHA lactate dehydrogenase A, ASCT2, also known as solute carrier family 1, member 5 (SLC1A5); SN2, also known as solute carrier family 38, member 5 (SLC38A5); MCT monocarboxylic transporters, GOT aspartate transaminase, GLUD1 glutamate dehydrogenase 1, GLS1 glutaminase 1, G6P glucose 6-phosphate, F6P fructose 6-phosphate, FBP fructose 1,6-phosphate, DHAP dihydroxyacetone phosphate, G3P glyceraldehyde 3-phosphate, 3PG 3-phosphoglycerate, αKG α-ketoglutarate, Asp aspartate, OAA oxaloacetate, TCA cycle tricarboxylic acid cycle. The graph was created with BioRender.com.