The Mechenism Research Of CD90 In Of Tumor Cell Stemness Maintenance And Immune Microenvironmnet Of Pancreatic Cancer

Pancreatic ductal adenocarcinoma?PDAC?is a highly aggressive disease with no effective therapies so far.Cancer cells,especially cancer stem cells?CSCs?redirect the immune cells to evade immune surveillance,and even co-opt immune cells to support their growth and metastasis.However,identification of CSCs and the biological process that mediates the crosstalk between immune cells and CSCs remain largely uncharacterized in PDAC.Here we found CD90 was expressed both on stromal and tumor cells,and its high expression was related to poor prognosis in PDAC patients.The CD90^highly-expressed subpopulation from PDAC harbored higher stemness features and tumorigenicity.Notably,CD90 could bind directly to the receptor CD11 b on the surface of monocytes/macrophages,thereby mediating the direct interaction of CD90^hi tumor cells with pancreatic stellate cells and monocytes/macrophages.Most importantly,the crosstalk between CD90^hi tumor cells and monocytes/macrophages fosters an immunosuppressive state of immune cells,which in turn serve to sustain the stemness and epithelial-mesenchymal transition?EMT?state of PDAC cells.Moreover,we also found that PD-L1 was expressed dominantly on CD90^hi PDAC cells,suggesting another strategy to evade immune surveillance for these CD90^hi tumor cells.Overall these findings provide an understanding of clinical relevance and biological significance of CD90 expression in PDAC cells,uncovering a novel mechanism for CD90^hi tumor cells to escape from immune surveillance in PDAC.