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10.1093/jmcb/mju047 http://scihub22266oqcxt.onion/10.1093/jmcb/mju047 C4401212!4401212!25503107     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Mol+Cell+Biol 2015 ; 7 (2): 143-53 Nephropedia Template TP {{tp|p=25503107|t=2015. Tumor-derived microvesicles mediate human breast cancer invasion through differentially glycosylated EMMPRIN |pdf=|usr=}}{{25503107}} gab.com Text Tumor-derived microvesicles mediate human breast cancer invasion through differentially glycosylated EMMPRIN JO: J Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=25503107 #FOAvip Tumor cells secrete not only a variety of soluble factors, but also extracellular vesicles that are known to support the establishment of a favorable tumor niche by influencing the surrounding stroma cells. Here we show that tumor-derived microvesicles (T-MV) also directly influence the tumor cells by enhancing their invasion in a both autologous and heterologous manner. Neither the respective vesicle-free supernatant nor MV from benign mammary cells mediate invasion. Uptake of T-MV is essential for the proinvasive effect. We further identify the highly glycosylated form of the extracellular matrix metalloproteinase inducer (EMMPRIN) as a marker for proinvasive MV. EMMPRIN is also present at high levels on MV from metastatic breast cancer patients in vivo. Anti-EMMPRIN strategies, such as MV deglycosylation, gene knockdown, and specific blocking peptides, inhibit MV-induced invasion. Interestingly, the effect of EMMPRIN-bearing MV is not mediated by matrix metalloproteinases but by activation of the p38/MAPK signaling pathway in the tumor cells. In conclusion, T-MV stimulate cancer cell invasion via a direct feedback mechanism dependent on highly glycosylated EMMPRIN. Twit Text FOAVip Tumor-derived microvesicles mediate human breast cancer invasion through differentially glycosylated EMMPRIN ????J Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=25503107 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25503107 #FOAvip English Wikipedia <ref>{{Cite pmid|25503107}}</ref> Tumor-derived microvesicles mediate human breast cancer invasion through differentially glycosylated EMMPRIN #MMPMID25503107 Menck K; Scharf C; Bleckmann A; Dyck L; Rost U; Wenzel D; Dhople VM; Siam L; Pukrop T; Binder C; Klemm F J Mol Cell Biol 2015[Apr]; 7 (2): 143-53 PMID25503107show ga Tumor cells secrete not only a variety of soluble factors, but also extracellular vesicles that are known to support the establishment of a favorable tumor niche by influencing the surrounding stroma cells. Here we show that tumor-derived microvesicles (T-MV) also directly influence the tumor cells by enhancing their invasion in a both autologous and heterologous manner. Neither the respective vesicle-free supernatant nor MV from benign mammary cells mediate invasion. Uptake of T-MV is essential for the proinvasive effect. We further identify the highly glycosylated form of the extracellular matrix metalloproteinase inducer (EMMPRIN) as a marker for proinvasive MV. EMMPRIN is also present at high levels on MV from metastatic breast cancer patients in vivo. Anti-EMMPRIN strategies, such as MV deglycosylation, gene knockdown, and specific blocking peptides, inhibit MV-induced invasion. Interestingly, the effect of EMMPRIN-bearing MV is not mediated by matrix metalloproteinases but by activation of the p38/MAPK signaling pathway in the tumor cells. In conclusion, T-MV stimulate cancer cell invasion via a direct feedback mechanism dependent on highly glycosylated EMMPRIN. äTumor-derived microvesicles mediate human breast cancer invasion throu(epmc).pdf DeepDyve Pubget Overpricing