. Author manuscript; available in PMC: 2016 Mar 21.

Published in final edited form as: Semin Cell Dev Biol. 2015 Aug 12;43:22–32. doi: 10.1016/j.semcdb.2015.08.002

Table 1.

Alteration of amino acid management pathways in cancer.

Amino acid metabolism

Gene	Function	Cancer alteration/relevance	References

GLS	Rate limiting step in glutaminolysis	Increased translational efficiency downstream of MYC, miR-23a/b	[58]
PHGDH	Rate limiting step in serine biosynthesis	Genomic amplification and over-expression	[23,24]
SHMT2	Diversion of serine into mitochondrial one-carbon metabolism	Over-expression, drives hypoxia resistance	[23,35,36]
GLDC	Key component of the glycine cleavage complex	Prevents toxic glycine accumulation, drives broad metabolic changes	[36,42]
ASNS	Asparagine biosynthesis	Increased expression in glioblastoma	[65]
Amino acid sensing

Gene	Function	Cancer alteration/relevance	References

mTOR	Protein kinase, controls translation in response to nutrient sufficiency signals	Activating point mutations, amino acid starvation fails to inactivate mTORC1	[120,155]
FLCN	mTORC1 positive regulator, GTPase activating protein for RAG C/D	Loss of function mutations in Birt–Hogg–Dubé syndrome	[105–107]
DEPDC5	GATOR1 component, negative regulator of mTORC1, GTPase activating protein for RAG A/B	Deletion of 22q12.2, amino acid starvation fails to inactivate mTORC1	[116,117]
NPRL2	GATOR1 component, negative regulator of mTORC1, GTPase activating protein for RAG A/B	Deletion of 3p21.3, amino acid starvation fails to inactivate mTORC1	[116,118,119]