Amino acid metabolism plays a crucial role in tumor biology and therapy. Amino acids contribute to tumorigenesis and tumor immunity by acting as nutrients, signaling molecules, and regulators of gene transcription and epigenetic modification. Targeting amino acid metabolism offers new therapeutic approaches after surgery, radiotherapy, and chemotherapy. This review summarizes recent progress in amino acid metabolism in malignancy, their interactions with signal pathways, and their effects on the tumor microenvironment and epigenetic modification. It highlights potential therapeutic applications and future directions. Amino acid metabolism is altered in tumors, challenging the traditional classification of essential and nonessential amino acids. Amino acids are pivotal regulators in tumors, participating in bidirectional interactions with signal pathways, tumor microenvironment, and epigenetic modifications. Clinical trials suggest that limiting amino acid intake may improve cancer prognosis. Key questions include determining the primary effect of amino acids on tumor progression, developing optimal strategies for amino acid-based therapies, and understanding the causal link between altered amino acid metabolism and tumor etiology. Amino acid metabolism in cancer is reprogrammed, with certain amino acids becoming essential in tumors. Glutamine, a conditional EAA, is crucial for tumor cells due to their high demand. It is the most abundant amino acid in plasma and rapidly consumed in tumor cells. Glutamine metabolism involves transporters like ASCT2 and enzymes like glutaminase (GLS1 and GLS2), which play opposite roles in tumor development. GLS1 is oncogenic, while GLS2 is a tumor suppressor. GLS1 is essential for tumor growth, invasion, and metastasis, while GLS2 regulates GSH/GSSG balance and promotes lipid ROS production, leading to ferroptosis. Arginine, another conditional EAA, is synthesized from aspartate and citrulline in the urea cycle. Its downregulation in cancer cells redirects aspartate towards pyrimidine biosynthesis, facilitating tumor proliferation. Arginine is transported via CAT family transporters and converted into polyamines, which promote tumor growth. Arginine can also produce NO, affecting TME and tumor proliferation. Branched-chain amino acids (BCAAs) are essential for protein synthesis and mTORC1 activation. BCAA metabolism involves enzymes like BCAT2, producing BCKA, which is further metabolized into acetyl-CoA and succinyl-CoA, participating in the TCA cycle. BCAAs also regulate nucleotide synthesis through RRM2. Tryptophan metabolism is crucial for tumor progression, with the kynurenine pathway producing kynurenine, which blocks T cell proliferation and induces T cell death. Kynurenine is further catabolized to NAD+ and alanine, promoting cancer progression. Tryptophan can also be metabolized via the 5-HT and indole pathways, affecting tumor growth and immune response. Asparagine and aspartAmino acid metabolism plays a crucial role in tumor biology and therapy. Amino acids contribute to tumorigenesis and tumor immunity by acting as nutrients, signaling molecules, and regulators of gene transcription and epigenetic modification. Targeting amino acid metabolism offers new therapeutic approaches after surgery, radiotherapy, and chemotherapy. This review summarizes recent progress in amino acid metabolism in malignancy, their interactions with signal pathways, and their effects on the tumor microenvironment and epigenetic modification. It highlights potential therapeutic applications and future directions. Amino acid metabolism is altered in tumors, challenging the traditional classification of essential and nonessential amino acids. Amino acids are pivotal regulators in tumors, participating in bidirectional interactions with signal pathways, tumor microenvironment, and epigenetic modifications. Clinical trials suggest that limiting amino acid intake may improve cancer prognosis. Key questions include determining the primary effect of amino acids on tumor progression, developing optimal strategies for amino acid-based therapies, and understanding the causal link between altered amino acid metabolism and tumor etiology. Amino acid metabolism in cancer is reprogrammed, with certain amino acids becoming essential in tumors. Glutamine, a conditional EAA, is crucial for tumor cells due to their high demand. It is the most abundant amino acid in plasma and rapidly consumed in tumor cells. Glutamine metabolism involves transporters like ASCT2 and enzymes like glutaminase (GLS1 and GLS2), which play opposite roles in tumor development. GLS1 is oncogenic, while GLS2 is a tumor suppressor. GLS1 is essential for tumor growth, invasion, and metastasis, while GLS2 regulates GSH/GSSG balance and promotes lipid ROS production, leading to ferroptosis. Arginine, another conditional EAA, is synthesized from aspartate and citrulline in the urea cycle. Its downregulation in cancer cells redirects aspartate towards pyrimidine biosynthesis, facilitating tumor proliferation. Arginine is transported via CAT family transporters and converted into polyamines, which promote tumor growth. Arginine can also produce NO, affecting TME and tumor proliferation. Branched-chain amino acids (BCAAs) are essential for protein synthesis and mTORC1 activation. BCAA metabolism involves enzymes like BCAT2, producing BCKA, which is further metabolized into acetyl-CoA and succinyl-CoA, participating in the TCA cycle. BCAAs also regulate nucleotide synthesis through RRM2. Tryptophan metabolism is crucial for tumor progression, with the kynurenine pathway producing kynurenine, which blocks T cell proliferation and induces T cell death. Kynurenine is further catabolized to NAD+ and alanine, promoting cancer progression. Tryptophan can also be metabolized via the 5-HT and indole pathways, affecting tumor growth and immune response. Asparagine and aspart