Tumor-associated macrophages (TAMs) play a critical role in the tumor microenvironment by modulating tumor progression, angiogenesis, invasion, metastasis, immunosuppression, and chemoresistance. These macrophages are classified into two main phenotypes: M1 (pro-inflammatory and antitumor) and M2 (anti-inflammatory and pro-tumorigenic). TAMs predominantly exhibit an M2-like phenotype and are closely associated with poor clinical outcomes, as their accumulation correlates with increased tumor growth, survival, and angiogenesis. TAMs are recruited to tumors through various mechanisms, including soluble factors such as cytokines, chemokines, and growth factors, as well as ECM components and hypoxia. Hypoxia promotes TAM recruitment and polarization toward a pro-tumorigenic phenotype by altering gene expression profiles and enhancing the secretion of pro-angiogenic factors like VEGF-A. TAMs also contribute to tumor invasion and metastasis by secreting proteolytic enzymes and modulating the tumor microenvironment. Additionally, TAMs support the formation of the pre-metastatic niche, which is essential for tumor cell colonization in distant organs. TAMs also mediate immunosuppression by secreting factors such as IL-10 and TGF-β, which inhibit T cell function and promote the recruitment of regulatory T cells. Furthermore, TAMs are involved in the self-renewal and chemoresistance of cancer stem cells. Targeting TAMs represents a promising strategy for cancer therapy, as interventions aimed at inhibiting TAM recruitment, converting TAMs to an M1 phenotype, or suppressing TAM survival may offer new therapeutic approaches. Current research highlights the importance of TAMs in cancer progression and suggests that reprogramming TAMs toward an antitumor M1 phenotype could be a key focus for future cancer therapies.Tumor-associated macrophages (TAMs) play a critical role in the tumor microenvironment by modulating tumor progression, angiogenesis, invasion, metastasis, immunosuppression, and chemoresistance. These macrophages are classified into two main phenotypes: M1 (pro-inflammatory and antitumor) and M2 (anti-inflammatory and pro-tumorigenic). TAMs predominantly exhibit an M2-like phenotype and are closely associated with poor clinical outcomes, as their accumulation correlates with increased tumor growth, survival, and angiogenesis. TAMs are recruited to tumors through various mechanisms, including soluble factors such as cytokines, chemokines, and growth factors, as well as ECM components and hypoxia. Hypoxia promotes TAM recruitment and polarization toward a pro-tumorigenic phenotype by altering gene expression profiles and enhancing the secretion of pro-angiogenic factors like VEGF-A. TAMs also contribute to tumor invasion and metastasis by secreting proteolytic enzymes and modulating the tumor microenvironment. Additionally, TAMs support the formation of the pre-metastatic niche, which is essential for tumor cell colonization in distant organs. TAMs also mediate immunosuppression by secreting factors such as IL-10 and TGF-β, which inhibit T cell function and promote the recruitment of regulatory T cells. Furthermore, TAMs are involved in the self-renewal and chemoresistance of cancer stem cells. Targeting TAMs represents a promising strategy for cancer therapy, as interventions aimed at inhibiting TAM recruitment, converting TAMs to an M1 phenotype, or suppressing TAM survival may offer new therapeutic approaches. Current research highlights the importance of TAMs in cancer progression and suggests that reprogramming TAMs toward an antitumor M1 phenotype could be a key focus for future cancer therapies.