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10.18632/oncotarget.16410 http://scihub22266oqcxt.onion/10.18632/oncotarget.16410 C5584171!5584171!28881585     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2017 ; 8 (31): 50582-93 Nephropedia Template TP {{tp|p=28881585|t=2017. C/EBP-? positively regulates MDSC expansion and endothelial VEGFR2 expression in tumor development |pdf=|usr=}}{{28881585}} gab.com Text C/EBP- positively regulates MDSC expansion and endothelial VEGFR2 expression in tumor development JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28881585 #FOAvip Vascular endothelial cells and Gr-1+CD11b+ myeloid derived suppressor cells (MDSCs) are two important components that constitute the tumor microenvironment. Targeting these cells offers the potential to halt tumor growth. In this study, we report a common mediator in C/EBP-? that regulates both components and aids in tumor development. C/EBP-? is elevated in tumor derived MDSCs. Interestingly, genetic deletion of C/EBP-? in mice significantly impaired MDSC expansion in response to tumor progression, but it had no effect on Gr-1+CD11b+ cell production in normal development. It suggests a specific role of C/EBP-? in emergency myelopoiesis under tumor conditions. Consistent with the pro tumor functions of MDSCs, loss of C/EBP-? resulted in reduced tumor angiogenesis and tumor growth. Moreover, we found expression of C/EBP-? in vascular endothelial cells. C/EBP-? regulated cell motility, endothelial network formation and vascular sprouting. Notably, inactivation of C/EBP-? in endothelial cells specifically inhibited the expression of VEGFR2 but not VEGFR1. Ectopic expression of C/EBP-? increased and knockdown of the gene decreased VEGFR2 expression. C/EBP-? is recruited to the promoter region of VEGFR2, indicative of transcriptional regulation. Collectively, this study has identified a positive mediator in C/EBP-?, which regulates tumor induced MDSC expansion and VEGFR2 expression in endothelium. Considering the importance of MDSCs and endothelial cells in tumor progression, targeting C/EBP-? may provide an interesting means for cancer therapy, killing two birds with one stone. Twit Text FOAVip C/EBP- positively regulates MDSC expansion and endothelial VEGFR2 expression in tumor development ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28881585 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28881585 #FOAvip English Wikipedia <ref>{{Cite pmid|28881585}}</ref> C/EBP-? positively regulates MDSC expansion and endothelial VEGFR2 expression in tumor development #MMPMID28881585 Min Y; Li J; Qu P; Lin PC Oncotarget 2017[Aug]; 8 (31): 50582-93 PMID28881585show ga Vascular endothelial cells and Gr-1+CD11b+ myeloid derived suppressor cells (MDSCs) are two important components that constitute the tumor microenvironment. Targeting these cells offers the potential to halt tumor growth. In this study, we report a common mediator in C/EBP-? that regulates both components and aids in tumor development. C/EBP-? is elevated in tumor derived MDSCs. Interestingly, genetic deletion of C/EBP-? in mice significantly impaired MDSC expansion in response to tumor progression, but it had no effect on Gr-1+CD11b+ cell production in normal development. It suggests a specific role of C/EBP-? in emergency myelopoiesis under tumor conditions. Consistent with the pro tumor functions of MDSCs, loss of C/EBP-? resulted in reduced tumor angiogenesis and tumor growth. Moreover, we found expression of C/EBP-? in vascular endothelial cells. C/EBP-? regulated cell motility, endothelial network formation and vascular sprouting. Notably, inactivation of C/EBP-? in endothelial cells specifically inhibited the expression of VEGFR2 but not VEGFR1. Ectopic expression of C/EBP-? increased and knockdown of the gene decreased VEGFR2 expression. C/EBP-? is recruited to the promoter region of VEGFR2, indicative of transcriptional regulation. Collectively, this study has identified a positive mediator in C/EBP-?, which regulates tumor induced MDSC expansion and VEGFR2 expression in endothelium. Considering the importance of MDSCs and endothelial cells in tumor progression, targeting C/EBP-? may provide an interesting means for cancer therapy, killing two birds with one stone. äC/EBP-? positively regulates MDSC expansion and endothelial VEGFR2 exp(epmc).pdf DeepDyve Pubget Overpricing