Amino acid metabolism plays a crucial role in tumor biology and therapy. Altered amino acid metabolism challenges the traditional classification of essential and nonessential amino acids, with non-essential amino acids becoming essential in tumors. Glutamine, arginine, branched-chain amino acids (BCAAs), tryptophan, asparagine, aspartate, serine, and glycine all contribute to tumor growth and immune evasion through various mechanisms. For instance, glutamine addiction is a hallmark of cancer cells, and targeting glutamine metabolism enzymes like ASCT2 and GLS1 can induce apoptosis in cancer cells. Arginine is essential for polyamine production, which facilitates cell proliferation and DNA stability. BCAAs are critical for protein synthesis and catabolism, with their levels influencing tumor progression. Tryptophan metabolism through the kynurenine pathway produces metabolites that block T cell proliferation and promote cancer metastasis. Asparagine and aspartate play roles in both tumor proliferation and metastasis, with asparagine being particularly important for distant metastatic colonization. Serine and glycine are essential for nucleotide synthesis, methylation, and redox homeostasis, contributing to tumor progression. Signal pathways such as mTOR, MYC, and KRAS also regulate amino acid metabolism, with mTOR acting as a convergence point for anabolism and catabolism, MYC upregulating key metabolic enzymes, and KRAS influencing glutamine metabolism. Macropinocytosis in the tumor microenvironment (TME) allows cancer cells to take up essential nutrients, while amino acid metabolism in the TME is influenced by the tumor's interactions with surrounding cells and the extracellular matrix. Targeting amino acid metabolism offers new therapeutic approaches for cancer treatment.Amino acid metabolism plays a crucial role in tumor biology and therapy. Altered amino acid metabolism challenges the traditional classification of essential and nonessential amino acids, with non-essential amino acids becoming essential in tumors. Glutamine, arginine, branched-chain amino acids (BCAAs), tryptophan, asparagine, aspartate, serine, and glycine all contribute to tumor growth and immune evasion through various mechanisms. For instance, glutamine addiction is a hallmark of cancer cells, and targeting glutamine metabolism enzymes like ASCT2 and GLS1 can induce apoptosis in cancer cells. Arginine is essential for polyamine production, which facilitates cell proliferation and DNA stability. BCAAs are critical for protein synthesis and catabolism, with their levels influencing tumor progression. Tryptophan metabolism through the kynurenine pathway produces metabolites that block T cell proliferation and promote cancer metastasis. Asparagine and aspartate play roles in both tumor proliferation and metastasis, with asparagine being particularly important for distant metastatic colonization. Serine and glycine are essential for nucleotide synthesis, methylation, and redox homeostasis, contributing to tumor progression. Signal pathways such as mTOR, MYC, and KRAS also regulate amino acid metabolism, with mTOR acting as a convergence point for anabolism and catabolism, MYC upregulating key metabolic enzymes, and KRAS influencing glutamine metabolism. Macropinocytosis in the tumor microenvironment (TME) allows cancer cells to take up essential nutrients, while amino acid metabolism in the TME is influenced by the tumor's interactions with surrounding cells and the extracellular matrix. Targeting amino acid metabolism offers new therapeutic approaches for cancer treatment.