Tumor-associated macrophages (TAMs) play a critical role in the tumor microenvironment by modulating tumor progression, angiogenesis, invasion, metastasis, immunosuppression, and chemoresistance. TAMs are primarily M2-polarized macrophages that support tumor growth and progression by creating a favorable microenvironment. They are recruited to tumors through various signals, including cytokines, chemokines, extracellular matrix components, and hypoxia. TAMs can shift from an M1-like phenotype in early tumor stages to an M2-like phenotype in advanced tumors, promoting immunosuppression and tumor progression. TAMs also contribute to tumor metastasis by facilitating cell invasion, promoting pre-metastatic niche formation, and supporting cancer stem cell self-renewal and chemoresistance. TAMs secrete factors that enhance angiogenesis, tumor survival, and immune evasion. Targeting TAMs is a promising strategy for cancer therapy, with approaches including inhibiting TAM recruitment, converting TAMs to M1-like macrophages, and suppressing TAM survival. Current research highlights the importance of TAMs in cancer progression and suggests that reprogramming TAMs toward an antitumor M1 phenotype could be a key therapeutic strategy.Tumor-associated macrophages (TAMs) play a critical role in the tumor microenvironment by modulating tumor progression, angiogenesis, invasion, metastasis, immunosuppression, and chemoresistance. TAMs are primarily M2-polarized macrophages that support tumor growth and progression by creating a favorable microenvironment. They are recruited to tumors through various signals, including cytokines, chemokines, extracellular matrix components, and hypoxia. TAMs can shift from an M1-like phenotype in early tumor stages to an M2-like phenotype in advanced tumors, promoting immunosuppression and tumor progression. TAMs also contribute to tumor metastasis by facilitating cell invasion, promoting pre-metastatic niche formation, and supporting cancer stem cell self-renewal and chemoresistance. TAMs secrete factors that enhance angiogenesis, tumor survival, and immune evasion. Targeting TAMs is a promising strategy for cancer therapy, with approaches including inhibiting TAM recruitment, converting TAMs to M1-like macrophages, and suppressing TAM survival. Current research highlights the importance of TAMs in cancer progression and suggests that reprogramming TAMs toward an antitumor M1 phenotype could be a key therapeutic strategy.