Tumor microenvironment (TME) plays a critical role in tumor development, metastasis, and immune evasion. TME-targeted therapy focuses on TME components, pathways, or molecules as therapeutic targets. Biomimetic nanocarriers with low clearance, low immunogenicity, and high targeting potential are promising for tumor treatment. This review discusses TME composition, including cancer-associated fibroblasts (CAFs), extracellular matrix (ECM), tumor vasculature, and non-tumor cells, and highlights the latest research on biomimetic nanoparticles (NPs) based on TME. It also discusses the opportunities and challenges of clinical translation of biomimetic NPs. TME is characterized by immunosuppression, and immunotherapy aims to restore antitumor activity and weaken immunosuppressive effects. TME differs significantly from normal cells, making it a target for safe and efficient tumor treatment. Nanoparticles can deliver anti-tumor drugs to tumor sites through EPR effects and targeting molecules, improving drug solubility, bioavailability, and reducing toxicity. However, nanoparticles can be cleared by the mononuclear phagocytic system (MPS), reducing efficacy. Biomimetic NPs, modified with cell membranes, exosomes, or proteins, avoid MPS clearance by mimicking "in vivo components." TME includes CAFs, ECM, tumor vasculature, and immune cells. CAFs are essential stromal cells, genetically stable, and less likely to develop resistance. Targeting CAFs can disrupt crosstalk with cancer cells, altering the tumor microenvironment and improving combined therapy. ECM provides physical support and regulates cell functions, and its disruption can affect tumor invasiveness. Tumor vasculature is structurally different from normal tissues, and vascular-targeted therapy inhibits angiogenesis, reducing tumor growth and metastasis. Immune cells in TME, including TAMs, DCs, T-cells, B-cells, NK cells, and MDSCs, are key components. TAMs have dual roles in tumor promotion and suppression, while DCs are potent antigen-presenting cells. Tregs inhibit immune responses, and targeting them can enhance anti-tumor activity. B-cells and NK cells also play roles in tumor immunity. MDSCs promote tumor growth through immunosuppressive mechanisms. Biomimetic NPs, such as erythrocyte membrane-coated NPs, tumor cell membrane-coated NPs, and immune cell membrane-coated NPs, improve targeting and reduce immune clearance. These NPs can deliver drugs, enhance immune responses, and modulate TME. For example, erythrocyte membrane-coated NPs improve circulation time and reduce clearance, while tumor cell membrane-coated NPs enhance cancer-specific accumulation. Macrophage membrane-coated NPs avoid MPS clearance and enhance drug delivery. NK cell membrane-coated NPs improve targetingTumor microenvironment (TME) plays a critical role in tumor development, metastasis, and immune evasion. TME-targeted therapy focuses on TME components, pathways, or molecules as therapeutic targets. Biomimetic nanocarriers with low clearance, low immunogenicity, and high targeting potential are promising for tumor treatment. This review discusses TME composition, including cancer-associated fibroblasts (CAFs), extracellular matrix (ECM), tumor vasculature, and non-tumor cells, and highlights the latest research on biomimetic nanoparticles (NPs) based on TME. It also discusses the opportunities and challenges of clinical translation of biomimetic NPs. TME is characterized by immunosuppression, and immunotherapy aims to restore antitumor activity and weaken immunosuppressive effects. TME differs significantly from normal cells, making it a target for safe and efficient tumor treatment. Nanoparticles can deliver anti-tumor drugs to tumor sites through EPR effects and targeting molecules, improving drug solubility, bioavailability, and reducing toxicity. However, nanoparticles can be cleared by the mononuclear phagocytic system (MPS), reducing efficacy. Biomimetic NPs, modified with cell membranes, exosomes, or proteins, avoid MPS clearance by mimicking "in vivo components." TME includes CAFs, ECM, tumor vasculature, and immune cells. CAFs are essential stromal cells, genetically stable, and less likely to develop resistance. Targeting CAFs can disrupt crosstalk with cancer cells, altering the tumor microenvironment and improving combined therapy. ECM provides physical support and regulates cell functions, and its disruption can affect tumor invasiveness. Tumor vasculature is structurally different from normal tissues, and vascular-targeted therapy inhibits angiogenesis, reducing tumor growth and metastasis. Immune cells in TME, including TAMs, DCs, T-cells, B-cells, NK cells, and MDSCs, are key components. TAMs have dual roles in tumor promotion and suppression, while DCs are potent antigen-presenting cells. Tregs inhibit immune responses, and targeting them can enhance anti-tumor activity. B-cells and NK cells also play roles in tumor immunity. MDSCs promote tumor growth through immunosuppressive mechanisms. Biomimetic NPs, such as erythrocyte membrane-coated NPs, tumor cell membrane-coated NPs, and immune cell membrane-coated NPs, improve targeting and reduce immune clearance. These NPs can deliver drugs, enhance immune responses, and modulate TME. For example, erythrocyte membrane-coated NPs improve circulation time and reduce clearance, while tumor cell membrane-coated NPs enhance cancer-specific accumulation. Macrophage membrane-coated NPs avoid MPS clearance and enhance drug delivery. NK cell membrane-coated NPs improve targeting