Modulating amino acid cross-talks with the host for cancer diagnosis and therapy

Cancer cells repurpose excess nitrogen for the anabolic synthesis of macromolecules required for tumour proliferation and growth. One selected strategy to maximize nitrogen levels is reprogramming metabolic routes to reduce protein catabolism and nitrogen disposal. The liver`s urea cycle (UC) is the primary metabolic pathway to convert excess nitrogen to disposable urea secreted in the urine. Outside the liver, UC enzymes are differentially expressed to accommodate cellular needs. Interestingly, in cancer, the expression of UC enzymes is altered to maximize nitrogen incorporation into biomass as amino and nucleic acids, thus supporting tumour growth and aggressiveness. The new flux of UC substrates into biosynthetic routes in the tumor alters the host metabolism. Hence, changes in the expression of UC enzymes in tumors and in the host may have diagnostic and prognostic implications for cancer diagnosis and outcome.