Abrogating <scp>GPT2</scp> in triple?negative breast cancer inhibits tumor growth and promotes autophagy

Uncontrolled proliferation and altered metabolic reprogramming are hallmarks of cancer. Active glycolysis glutaminolysis characteristic features these required for tumorigenesis. A fine balance between cancer metabolism autophagy is a prerequisite homeostasis within cells. Here we show that glutamate pyruvate transaminase 2 (GPT2), which serves as pivot glutaminolysis, highly upregulated in aggressive breast cancers, particularly the triple-negative subtype. Abrogation this enzyme results decreased tricarboxylic acid cycle intermediates, promotes rewiring glucose carbon atoms alterations nutrient levels. Concordantly, loss GPT2 an impairment mechanistic target rapamycin complex 1 activity well induction autophagy. Furthermore, vivo xenograft studies have shown correlates with tumor growth markers induced correlate low levels patient samples. Taken together, findings indicate cells close network sensing pathways necessary to sustain tumorigenesis aminotransferase reactions play important role maintaining balance.