CD73-deficient mice are resistant to carcinogenesis.

摘要: CD73 is a cell surface 5'-nucleotidase that converts AMP to adenosine, an immune suppressive molecule. may promote escape in cancer by contributing the degradation of extracellular ATP released dying cells hypoxic tumors or following chemotherapy. However, whether exerts critical oncogenic function during tumorigenesis unknown. In this study, we used genetically deficient mice investigate its contribution autochthonous tumor formation. deficiency suppressed development 3-methylcholanthrene (MCA)-induced fibrosarcomas through mechanism relying upon IFN-γ, natural killer (NK) cells, and CD8(+) T cells. Similarly, also prostate TRAMP transgenic mice. Importantly, treatment with anti-CD73 monoclonal antibody effectively growth established MCA-induced TRAMP-C1 inhibited lung metastases. The therapeutic activity against primary was dependent on whereas antimetastatic host expression independent NK Taken together, our findings indicate factor antibodies offer novel generalized strategy blunt treat cancer.