Figure 2.

Glutamine consumption is increased in most tumors. During tumorigenesis, glucose derived lactate is increased, and at the same time, contribution of glucose to TCA is decreased. Accompanied with glucose metabolism change, glutamine metabolism is up-regulated to compensate energy and macromolecular for cell proliferation and growth. p53 is mutated, while MYC is overexpressed, which promotes glutamine metabolism by upregulating GLS1 activity during tumorigenesis. GLS1 is highly expressed in many tumors and promotes tumor proliferation. In contrast, GLS2 expression is reduced in some tumors. GLS, glutaminase; TCA, tricarboxylic acid cycle. Bold arrow, increased glutamine metabolism, decreased glucose metabolism and mutated MYC; dashed line, tumorigenesis procedure.