Tumor cells usually secrete soluble factors to improve their proliferation via autocrine network or to escape from immune surveillance by inhibiting antitumor immunity,among these factors IL-10 and IL-6 play more important roles. Since both cytokines’ signal transductions are mediated through the STAT3 pathway,STAT3 becomes an attractive target for tumor therapy. In present study,STAT3 of murine tumor cell lines B16 and MCA-38 was constitutively activated. After treatment with STAT3-decoy ODN,the proliferation of these tumor cells was inhibited and the transcription of IL-10 or IL-6 in tumor cells was down-regulated. These results suggested that STAT3 is a good target candidate,and STAT3-decoy ODN may possibly be used as a strategy for breaking both tumor autocrine network and tumor immunotolerance.
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机译：Derazantinib, a fibroblast growth factor receptor inhibitor, inhibits colony-stimulating factor receptor-1 in macrophages and tumor cells and in combination with a murine programmed cell death ligand-1-antibody activates the immune environment of murine syngeneic tumor models
机译：Macrophages that have ingested apoptotic cells in vitro inhibit proinflammatory cytokine production through autocrine/paracrine mechanisms involving TGF-beta, PGE2, and PAF.
