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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Mol+Cell+Biol
2015 ; 7
(2
): 143-53
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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
PMID25503107
show 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.