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Cited by 668

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Endothelial expression of autocrine VEGF upon the uptake of tumor-derived microvesicles containing oncogenic EGFR

Open access
Al-Nedawi, Khalid, Meehan, Brian, Kerbel, Robert S., Allison, Anthony C., Rak, Janusz·2009·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.0804543106
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Abstract

Activated EGF receptor (EGFR) plays an oncogenic role in several human malignancies. Although the intracellular effects of EGFR are well studied, its ability to induce and modulate tumor angiogenesis is less understood. We found previously that oncogenic EGFR can be shed from cancer cells as cargo of membrane microvesicles (MVs), which can interact with surfaces of other cells. Here we report that MVs produced by human cancer cells harboring activated EGFR (A431, A549, DLD-1) can be taken up by cultured endothelial cells, in which they elicit EGFR-dependent responses, including activation of MAPK and Akt pathways. These responses can be blocked by annexin V and its homodimer, Diannexin, both of which cloak phosphatidylserine residues on the surfaces of MVs. Interestingly, the intercellular EGFR transfer is also accompanied by the onset of VEGF expression in endothelial cells and by autocrine activation of its key signaling receptor (VEGF receptor-2). In A431 human tumor xenografts in mice, angiogenic endothelial cells stain positively for human EGFR and phospho-EGFR, while treatment with Diannexin leads to a reduction of tumor growth rate and microvascular density. Thus, we propose that oncogene-containing tumor cell-derived MVs could act as a unique form of angiogenesis-modulating stimuli and are capable of switching endothelial cells to act in an autocrine mode.

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Metadata

Authors
Al-Nedawi, K., Meehan, B., Kerbel, R. S., Allison, A. C., & Rak, J.
Venue
Proceedings of the National Academy of Sciences
Publisher
Proceedings of the National Academy of Sciences
Published
2009-03-10
Volume
106
Issue
10
Pages
3794-3799
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.0804543106
OpenAlex
W1984557698
Cited by
668
References
3
FWCI
12.00
Type
journal article
Language
en
Open access
green

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