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10.18632/oncotarget.23020 http://scihub22266oqcxt.onion/10.18632/oncotarget.23020 29383101!5777713!29383101     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29383101&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Oncotarget 2017 ; 8 (70): 114554-114567 Nephropedia Template TP {{tp|p=29383101|t=2017. CXCR2(+) MDSCs promote breast cancer progression by inducing EMT and activated T cell exhaustion |pdf=|usr=}}{{29383101}} gab.com Text CXCR2(+) MDSCs promote breast cancer progression by inducing EMT and activated T cell exhaustion JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=29383101 #FOAvip Although myeloid-derived suppressor cells (MDSCs) have been demonstrated to contribute to tumor initiation, progression and metastasis, however, which MDSC subsets are preferentially expanded and activated, and what's the key molecular mechanism responsible for specific MDSC subsets in promoting tumor progression need to be fully addressed. Here we identify that Ly6G(mi)Ly6C(lo)CD11b(+)CXCR2(+) subpopulation (named CXCR2(+) MDSCs) are predominately expanded and recruited in systemic and local tumor microenvironment during breast cancer progression and metastasis. The proportion of CXCR2(+) MDSCs is inversely correlated with the infiltration of CD4(+) or CD8(+) T cells. Besides, CXCR2(+) MDSCs promote breast cancer growth and metastasis to lung and/or lymph node in vivo. Furthermore, CXCR2(+) MDSCs induce epithelial mesenchymal transition (EMT) of breast cancer cells via IL-6. Moreover, CXCR2(+) MDSCs upregulate the expression of immunosuppressive molecules programmed cell death protein 1(PD1), PD1 ligand 1 (PDL1), lymphocyte activation gene 3 protein (LAG3), cytotoxic T lymphocyte antigen 4 (CTLA4), and T cell immunoglobulin domain and mucin domain protein 3 (TIM3) on CD4(+) or CD8(+) T cells, and induce exhaustion of the activated T cells partially via IFN-gamma. These results demonstrate that CXCR2(+) MDSCs accelerate breast cancer progression via directly inducing cancer cell EMT and indirectly promoting T cell exhaustion, suggesting that CXCR2(+) MDSCs may be a potential therapeutic target of breast cancer. Twit Text FOAVip CXCR2(+) MDSCs promote breast cancer progression by inducing EMT and activated T cell exhaustion ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=29383101 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29383101 #FOAvip English Wikipedia <ref>{{Cite pmid|29383101}}</ref> CXCR2(+) MDSCs promote breast cancer progression by inducing EMT and activated T cell exhaustion #MMPMID29383101 Zhu H; Gu Y; Xue Y; Yuan M; Cao X; Liu Q Oncotarget 2017[Dec]; 8 (70): 114554-114567 PMID29383101show ga Although myeloid-derived suppressor cells (MDSCs) have been demonstrated to contribute to tumor initiation, progression and metastasis, however, which MDSC subsets are preferentially expanded and activated, and what's the key molecular mechanism responsible for specific MDSC subsets in promoting tumor progression need to be fully addressed. Here we identify that Ly6G(mi)Ly6C(lo)CD11b(+)CXCR2(+) subpopulation (named CXCR2(+) MDSCs) are predominately expanded and recruited in systemic and local tumor microenvironment during breast cancer progression and metastasis. The proportion of CXCR2(+) MDSCs is inversely correlated with the infiltration of CD4(+) or CD8(+) T cells. Besides, CXCR2(+) MDSCs promote breast cancer growth and metastasis to lung and/or lymph node in vivo. Furthermore, CXCR2(+) MDSCs induce epithelial mesenchymal transition (EMT) of breast cancer cells via IL-6. Moreover, CXCR2(+) MDSCs upregulate the expression of immunosuppressive molecules programmed cell death protein 1(PD1), PD1 ligand 1 (PDL1), lymphocyte activation gene 3 protein (LAG3), cytotoxic T lymphocyte antigen 4 (CTLA4), and T cell immunoglobulin domain and mucin domain protein 3 (TIM3) on CD4(+) or CD8(+) T cells, and induce exhaustion of the activated T cells partially via IFN-gamma. These results demonstrate that CXCR2(+) MDSCs accelerate breast cancer progression via directly inducing cancer cell EMT and indirectly promoting T cell exhaustion, suggesting that CXCR2(+) MDSCs may be a potential therapeutic target of breast cancer. ?CXCR2(+) MDSCs promote breast cancer progression by inducing EMT and a(epmc).pdf DeepDyve Pubget Overpricing