As an important part of tumor microenvironment, tumor associated macrophages (TAMs) play a vital role in the occurrence, development, invasion, and metastasis of many malignant tumors and can significantly promote the formation of tumor blood vessels and lymphatic vessels, hence TAMs are greatly associated with poor prognosis. The research on nanomedicine has achieved huge progress, and nano-drugs have been widely utilized to treat various diseases through different mechanisms. Therefore, developing nano-drugs that are based on TAMs-associated anti-tumor mechanisms to effectively suppress tumor growth is expected to be a promising research filed. This paper introduces relevant information about TAMs in terms of their origin, and their roles in tumor genesis, development and metastasis. Furthermore, TAMs-related anti-tumor nano-drugs are summarized. Specifically, a wide range of nano-drugs targeting at TAMs are introduced, and categorized according to their therapeutic mechanisms toward tumors. Additionally, various nano delivery platforms using TAMs as cell carriers which aim at inhibiting tumor growth are reviewed. These two parts elucidate that the exploration of nanomedicine is essential to the study on TAMs-related anti-tumor strategies. This review is also intended to provide novel ideas for in-depth investigation on anti-tumor molecular mechanisms and nano-drug delivery systems based on TAMs.
NPs bind to retraction fibers and migrasomes during tumor cell migration. Such Nano–ECM interactions could alter cell morphology, limit cell motion range, change cell adhesion and inhibit tumor cell metastasis in vitro and in vivo.
To determine whether two-step ablation using sequential low and high temperature heating can achieve improved outcomes in animal tumor models when combined with chemotherapeutic liposomes (LP).
Intracellular delivery crossing the endomembrane barrier is the “last mile to target” for nano delivery systems carrying biomacromolecules, including genetic medicines. Nevertheless, a mass of nanomedicines is currently restricted by their equivocal safety and delivery efficiency. Here, we trimmed nano delivery at the cell perspective and established a general strategy independent of nanomaterials. Such a policy broadly facilitates the intracellular delivery of all kinds of tested nanomedicines, subtly by inducing ARF6 GTPases to their overactivated GTP-bound state. We discovered that ARF6, one member of ARF subfamily in small GTPases, regulated intracellular vesicle transport and lipid metabolism through GTP/GDP conversion. More importantly, we demonstrated that ARF6 biased to GTP-bound form induced GTPase overactivation, promoting endocytosis and reducing exocytosis of cargoes, including transferrin proteins and eleven types of nanogranules. This universal effect was mechanistically derived from forming a particular category of hybrid endosomes triggered by overactivated ARF6 via regulating cholesterol-associated vesicles and lipid raft/caveolae pathways. Cargoes were steadily and slowly delivered to the cytoplasm due to the mild microenvironment in hybrid endosomes. Based on these findings, we identified that QS11, a safe small molecule inhibitor of ARF GTPase-activating proteins, enhanced the antitumor efficacy of siEGFR-loaded nanoparticles by inducing ARF6 overactivation. In sum, it demonstrates that the tactics of tuning ARF6 GTPases to GTP-bound form will widely benefit cellular nano delivery.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.