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

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 (2014)

Bottom Line: Uptake of T-MV is essential for the proinvasive effect.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Hematology/Oncology, University Medical Center Göttingen, 37099 Göttingen, Germany.

No MeSH data available.


Related in: MedlinePlus

T-EV induce breast cancer invasion. (A) Electron microscopy (TEM) of T-MV and T-Exo. (B) Microinvasion assay of MCF-7 breast cancer cells stimulated with T-MV, T-Exo, and MV from normal epithelial cells (hTERT-MV) (all at 1 µg/ml), as well as the respective particle-free supernatants (sn) (mean ± SD, n = 3, *P < 0.001). Suffix M: vesicles/supernatant from MCF-7 cells; S: SK-BR-3; MDA: MDA-MB231; hTERT: hTERT-HME1. (C) Comparative analysis of cell invasion of MCF-7 and benign hTERT-HME1 cells stimulated with MV (10 µg/ml) (mean ± SD, n = 3, *P < 0.001).
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MJU047F1: T-EV induce breast cancer invasion. (A) Electron microscopy (TEM) of T-MV and T-Exo. (B) Microinvasion assay of MCF-7 breast cancer cells stimulated with T-MV, T-Exo, and MV from normal epithelial cells (hTERT-MV) (all at 1 µg/ml), as well as the respective particle-free supernatants (sn) (mean ± SD, n = 3, *P < 0.001). Suffix M: vesicles/supernatant from MCF-7 cells; S: SK-BR-3; MDA: MDA-MB231; hTERT: hTERT-HME1. (C) Comparative analysis of cell invasion of MCF-7 and benign hTERT-HME1 cells stimulated with MV (10 µg/ml) (mean ± SD, n = 3, *P < 0.001).

Mentions: EV from the breast cancer cell lines MCF-7 (T-EVM), SK-BR-3 (T-EVS), and MDA-MB231 (T-EVMDA), as well as the benign, immortalized mammary epithelial cell line hTERT-HME1 (hTERT-EV) were prepared by differential centrifugation without any previous stimulation. Upon transmission electron microscopy (TEM), the MV fraction consisted of a heterogeneous population of membrane-enclosed vesicles with a diameter of 100 up to 1000 nm, which clearly differed from the population of smaller, typically cup-shaped Exo (Figure 1A). There was no evidence of apoptotic bodies or cell debris.Figure 1


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

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 (2014)

T-EV induce breast cancer invasion. (A) Electron microscopy (TEM) of T-MV and T-Exo. (B) Microinvasion assay of MCF-7 breast cancer cells stimulated with T-MV, T-Exo, and MV from normal epithelial cells (hTERT-MV) (all at 1 µg/ml), as well as the respective particle-free supernatants (sn) (mean ± SD, n = 3, *P < 0.001). Suffix M: vesicles/supernatant from MCF-7 cells; S: SK-BR-3; MDA: MDA-MB231; hTERT: hTERT-HME1. (C) Comparative analysis of cell invasion of MCF-7 and benign hTERT-HME1 cells stimulated with MV (10 µg/ml) (mean ± SD, n = 3, *P < 0.001).
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4401212&req=5

MJU047F1: T-EV induce breast cancer invasion. (A) Electron microscopy (TEM) of T-MV and T-Exo. (B) Microinvasion assay of MCF-7 breast cancer cells stimulated with T-MV, T-Exo, and MV from normal epithelial cells (hTERT-MV) (all at 1 µg/ml), as well as the respective particle-free supernatants (sn) (mean ± SD, n = 3, *P < 0.001). Suffix M: vesicles/supernatant from MCF-7 cells; S: SK-BR-3; MDA: MDA-MB231; hTERT: hTERT-HME1. (C) Comparative analysis of cell invasion of MCF-7 and benign hTERT-HME1 cells stimulated with MV (10 µg/ml) (mean ± SD, n = 3, *P < 0.001).
Mentions: EV from the breast cancer cell lines MCF-7 (T-EVM), SK-BR-3 (T-EVS), and MDA-MB231 (T-EVMDA), as well as the benign, immortalized mammary epithelial cell line hTERT-HME1 (hTERT-EV) were prepared by differential centrifugation without any previous stimulation. Upon transmission electron microscopy (TEM), the MV fraction consisted of a heterogeneous population of membrane-enclosed vesicles with a diameter of 100 up to 1000 nm, which clearly differed from the population of smaller, typically cup-shaped Exo (Figure 1A). There was no evidence of apoptotic bodies or cell debris.Figure 1

Bottom Line: Uptake of T-MV is essential for the proinvasive effect.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Hematology/Oncology, University Medical Center Göttingen, 37099 Göttingen, Germany.

No MeSH data available.


Related in: MedlinePlus