Cancer treatment remains challenging due to the complexity of the tumor microenvironment, which promotes tumor heterogeneity and contributes to the development of multidrug resistance, ultimately hindering drug delivery and reducing therapeutic efficacy. In recent years, biomimetic nanocarriers have emerged as promising tools to address these challenges. Among them, cancer cell membrane (CCM)-coated nanoparticles (CCM-NPs) have attracted increasing attention due to their unique advantages, including homologous targeting, prolonged circulation mediated by self-recognition, and enhanced tumor penetration. Moreover, CCM-NPs can serve as versatile platforms for tumor vaccines by leveraging their inherent tumor-associated antigens and immunomodulatory potential. By leveraging CCMs to functionalize NPs, researchers have developed innovative approaches to improve drug delivery, enhance tumor immunotherapy, and optimize cancer vaccine efficacy. Despite these advancements, a comprehensive review summarizing the latest progress in CCM-based biomimetic nanocarriers for tumor treatment is lacking. This review integrates recent advances in CCM-NPs for targeted drug delivery and cancer vaccination, and discusses their fabrication, characterization, mechanisms and applications across multiple cancer types, which provides timely insights to guide their future development in precision tumor therapy.

The efficacy of immunotherapy is diminished by the low survival rate of effector CD8 + T cells after they have exerted their antitumor effects. Recent studies indicate that ammonia, generated from glutamine metabolism, accumulates in effector CD8 + T cells and triggers their apoptosis. These findings offer a comprehensive mechanistic understanding of effector T-cell mortality from a metabolic viewpoint, presenting novel opportunities for improving T-cell-mediated anticancer treatments.

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy characterized by a dense extracellular matrix (ECM) and a uniquely immunosuppressive tumor microenvironment (TME), which together form a formidable barrier that hinders deep drug penetration, limiting the efficacy of conventional therapies and leading to poor patient outcomes. Nanocarrier technology emerges as a promising strategy to improve treatment efficacy in PDAC. Nanocarriers can not only improve drug penetration through their adjustable physicochemical properties but also effectively regulate immune cell function in pancreatic cancer TME and promote anti-tumor immune response. This mini-review discusses the effects of nanocarriers on the immune microenvironment of PDAC, analyzing their mechanisms in modulating immune cells, overcoming ECM barriers, and reshaping the TME.

Ammonia, a by-product of glutamine metabolism, has emerged as a key immunometabolic regulator in the tumor microenvironment. Recent studies reveal that excessive ammonia accumulation impairs effector CD8+ T cell viability through a distinct form of organelle-centered cell death, characterized by lysosomal alkalinization, mitochondrial dysfunction, and autophagy inhibition. This phenomenon, termed ammonia-induced cell death (AICD), contributes to immune suppression and tumor progression. Here, we comprehensively review the molecular pathways governing ammonia production, transport, and detoxification, with a focus on the roles of GLS1, CPS1, Rh-family transporters, and associated solute carriers. We further highlight advances in chemical biology tools—such as ammonia-sensitive probes and isotope-labeled metabolomics—that enable the functional dissection of ammonia metabolism in immune and tumor cells. Emerging therapeutic strategies that combine ammonia metabolism modulators with immune checkpoint inhibitors offer promising avenues to enhance anti-tumor immunity. Despite recent progress, key challenges remain, including the incomplete understanding of ammonia clearance in T cells, limited data on other immune cell types, and concerns about metabolic toxicity. Targeting AICD thus represents a chemically tractable and clinically relevant approach at the interface of metabolism, immunity, and cancer therapy.

Triple-negative breast cancer (TNBC) is an aggressive and heterogeneous subtype lacking effective targeted therapies. Its tumor microenvironment (TME) exhibits distinct features, including acidity, redox imbalance, elevated reactive oxygen species (ROS), and hypoxia, which provide exploitable triggers for targeted drug delivery. Stimuli-responsive polymeric nanocarriers have emerged as promising platforms that enable spatiotemporally controlled and site-specific therapeutic release in response to these endogenous cues, as well as exogenous stimuli such as temperature and light. These systems improve drug accumulation, penetration, and therapeutic efficacy while reducing systemic toxicity. Unlike previous reviews that broadly discuss nanocarriers in cancer therapy, this review focuses on the structure–function relationships of TME-responsive polymeric systems in TNBC and their translational limitations. We summarize recent advances in pH-, redox-, ROS-, hypoxia-, photo- and temperature-responsive polymers, highlighting their design strategies and therapeutic applications. Key challenges, including stimulus heterogeneity, limited in vivo validation, and clinical translation barriers, are also discussed. This review provides a concise framework for the rational design of programmable, multi-responsive polymeric nanomedicines for TNBC therapy.