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Tumor-derived microvesicles mediate human breast cancer invasion through differentially glycosylated EMMPRIN.


ABSTRACT: 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.

SUBMITTER: Menck K 

PROVIDER: S-EPMC4401212 | biostudies-literature | 2015 Apr

REPOSITORIES: biostudies-literature

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Tumor-derived microvesicles mediate human breast cancer invasion through differentially glycosylated EMMPRIN.

Menck Kerstin K   Scharf Christian C   Bleckmann Annalen A   Dyck Lydia L   Rost Ulrike U   Wenzel Dirk D   Dhople Vishnu M VM   Siam Laila L   Pukrop Tobias T   Binder Claudia C   Klemm Florian F  

Journal of molecular cell biology 20141211 2


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  ...[more]

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