Cargo-eliminated osteosarcoma-derived small extracellular vesicles mediating competitive cellular uptake for inhibiting pulmonary metastasis of osteosarcoma.

Osteosarcoma (OS) derived small extracellular vesicles (OS-sEVs) have been shown to induce the formation of cancer-associated fibroblasts (CAFs), characterized by elevated pro-inflammatory factor expression and enhanced migratory and contractile abilities. These CAFs play a crucial role in priming lung metastasis by orchestrating the pre-metastatic niche (PMN) in the lung. Disrupting the communication between OS-sEVs and lung fibroblasts (LFs) emerges as a potent strategy to hinder OS pulmonary metastasis.

Glycan-Lectin interactions between platelets and tumor cells drive hematogenous metastasis.

Glycosylation is a ubiquitous cellular or microenvironment-specific post-translational modification that occurs on the surface of normal cells and tumor cells. Tumor cell-associated glycosylation is involved in hematogenous metastasis. A wide variety of tumors undergo aberrant glycosylation to interact with platelets.

[Progress in functions and mechanisms of immunosuppressive neutrophil subsets: An update].

Neutrophils are the most abundant circulating leukocytes in healthy adults, serving as the first-line defense against infections. In the last few years, scientists have reported neutrophils of immune suppressive properties, such as tumor-associated neutrophils (TAN) and low-density neutrophils (LDN). These neutrophils are found to be involved in many physiological and pathological conditions owing to their ability of regulating T cell functions and promoting angiogenesis and tumor growth through a number of mechanisms, including PD-1/PD-L1, antigen presentation, reactive oxygen species (ROS), arginase-1 (Arg1), inducible nitric oxide synthase (iNOS), etc.