English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

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

Menck, K., Scharf, C., Bleckmann, A., Dyck, L., Rost, U., Wenzel, D., et al. (2015). Tumor-derived microvesicles mediate human breast cancer invasion through differentially glycosylated EMMPRIN. Journal of Molecular Cell Biology, 7(2), 143-153. doi:10.1093/jmcb/mju047.

Item is

Basic

show hide
Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0027-A69F-7 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002A-1CAE-5
Genre: Journal Article

Files

show Files
hide Files
:
2166613.pdf (Publisher version), 719KB
Name:
2166613.pdf
Description:
-
Visibility:
Public
MIME-Type / Checksum:
application/pdf / [MD5]
Technical Metadata:
Copyright Date:
-
Copyright Info:
-
:
2166613_Suppl.pdf (Supplementary material), 2MB
Name:
2166613_Suppl.pdf
Description:
-
Visibility:
Public
MIME-Type / Checksum:
application/pdf / [MD5]
Technical Metadata:
Copyright Date:
-
Copyright Info:
-
License:
-

Locators

show
hide
Description:
-

Creators

show
hide
 Creators:
Menck, K., Author
Scharf, C., Author
Bleckmann, A., Author
Dyck, L., Author
Rost, U., Author
Wenzel, D.1, Author              
Dhople, V. M., Author
Siam, L., Author
Pukrop, T., Author
Binder, C., Author
Klemm, F., Author
Affiliations:
1Facility for Electron Microscopy, MPI for biophysical chemistry, Max Planck Society, ou_578615              

Content

show
hide
Free keywords: breast cancer; microvesicles; invasion; EMMPRIN; glycosylation
 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 autologousand 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.

Details

show
hide
Language(s): eng - English
 Dates: 2014-12-112015-04
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Method: Peer
 Identifiers: DOI: 10.1093/jmcb/mju047
 Degree: -

Event

show

Legal Case

show

Project information

show

Source 1

show
hide
Title: Journal of Molecular Cell Biology
Source Genre: Journal
 Creator(s):
Affiliations:
Publ. Info: -
Pages: - Volume / Issue: 7 (2) Sequence Number: - Start / End Page: 143 - 153 Identifier: -