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Extracellular vesicle secretion of miR-142-3p from lung adenocarcinoma cells induces tumor promoting changes in the stroma through cell-cell communication.
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- Additional Information
- Source:
Publisher: Wiley-Liss Country of Publication: United States NLM ID: 8811105 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1098-2744 (Electronic) Linking ISSN: 08991987 NLM ISO Abbreviation: Mol Carcinog Subsets: MEDLINE
- Publication Information:
Publication: <2005- > : [Hoboken, N.J.] : Wiley-Liss
Original Publication: New York : Alan R. Liss, Inc., c1988-
- Subject Terms:
- Abstract:
Extracellular vesicles (EVs) are mediators of communication between cancer cells and the surrounding tumor microenvironment. EV content is able to influence key tumorigenic changes including invasion, metastasis, and inducing pro-tumor changes in the stroma. MiR-142-3p is a known tumor suppressor in LAC and was recently shown to be enriched within LAC EVs, indicating its potential as a key signaling miRNA. Our research demonstrates the role EV associated miR-142-3p plays when transferred from LAC cells to both endothelial and fibroblast cells. We demonstrate that transfer of miR-142-3p in LAC EVs to endothelial cells promotes angiogenesis through inhibition of TGFβR1. Additionally, we show EV associated miR-142-3p promotes the cancer-associated fibroblast phenotype in lung fibroblast cells which we show is independent of TGFβ signaling. These findings suggest that miR-142-3p within LAC EVs can be transferred from LAC cells to both endothelial and fibroblast cells to promote tumor associated changes.
(© 2018 Wiley Periodicals, Inc.)
- Grant Information:
1002 International Terry Fox Research Institute (Early Detection of Lung Cancer-A Pan-Canadian Study)
- Contributed Indexing:
Keywords: MiRNA; NSCLC; exosomes; extracellular vesicles; lung adenocarcinoma
- Accession Number:
0 (Carcinogens)
0 (MIRN142 microRNA, human)
0 (MicroRNAs)
- Publication Date:
Date Created: 20181027 Date Completed: 20190708 Latest Revision: 20190708
- Publication Date:
20231215
- Accession Number:
10.1002/mc.22935
- Accession Number:
30362621
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