Dysregulated amino acid sensing drives colorectal cancer growth and metabolic reprogramming leading to chemoresistance.

CRC is a devastating disease highly modulated by dietary nutrients. mTORC1 contributes to tumor growth and limits therapy responses. Growth factor signaling is a major mechanism of mTORC1 activation. However, compensatory pathways exist to sustain mTORC1 activity following therapies that target oncogenic growth factor signaling. Amino acids potently activate mTORC1 via amino acid sensing GTPase activity towards Rags complexes (GATOR). The role of amino acid sensing pathways in CRC is unclear.

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