Display options
Cite
Lawson J, Dickman C, MacLellan S, et al. Selective secretion of microRNAs from lung cancer cells via extracellular vesicles promotes CAMK1D-mediated tube formation in endothelial cells. Oncotarget. 2017;8(48):83913-83924doi: 10.18632/oncotarget.19996.
Lawson, J., Dickman, C., MacLellan, S., Towle, R., Jabalee, J., Lam, S., & Garnis, C. (2017). Selective secretion of microRNAs from lung cancer cells via extracellular vesicles promotes CAMK1D-mediated tube formation in endothelial cells. Oncotarget, 8(48), 83913-83924. https://doi.org/10.18632/oncotarget.19996
Lawson, James, et al. "Selective secretion of microRNAs from lung cancer cells via extracellular vesicles promotes CAMK1D-mediated tube formation in endothelial cells." Oncotarget vol. 8,48 (2017): 83913-83924. doi: https://doi.org/10.18632/oncotarget.19996
Lawson J, Dickman C, MacLellan S, Towle R, Jabalee J, Lam S, Garnis C. Selective secretion of microRNAs from lung cancer cells via extracellular vesicles promotes CAMK1D-mediated tube formation in endothelial cells. Oncotarget. 2017 Aug 07;8(48):83913-83924. doi: 10.18632/oncotarget.19996. eCollection 2017 Oct 13. PMID: 29137392; PMCID: PMC5663564.
Copy Download .nbib Format: NLM
Share it on

Oncotarget. 2017 Aug 07;8(48):83913-83924. doi: 10.18632/oncotarget.19996. eCollection 2017 Oct 13.

Selective secretion of microRNAs from lung cancer cells via extracellular vesicles promotes CAMK1D-mediated tube formation in endothelial cells.

Oncotarget

James Lawson, Christopher Dickman, Sara MacLellan, Rebecca Towle, James Jabalee, Stephen Lam, Cathie Garnis

Affiliations

  1. Department of Integrative Oncology, British Columbia Cancer Research Centre, Vancouver, BC, Canada.
  2. Division of Otolaryngology, Department of Surgery, University of British Columbia, Vancouver, BC, Canada.

PMID: 29137392 PMCID: PMC5663564 DOI: 10.18632/oncotarget.19996

Abstract

Extracellular vesicles (EVs) are key signaling mediators between cancer cells and their supporting stroma, and regulate critical processes such as invasion, metastases, and angiogenesis. We have identified a subset of miRNAs (miR-142-3p, miR-143-3p, miR-145-5p, miR-150-5p, miR-223-3p, miR-451a, miR-486-5p, miR-605-5p) that are enriched in lung adenocarcinoma extracellular vesicles compared to the donor cells from which they were derived. Two well-known tumor suppressors, miR-143-3p and miR-145-5p, were also enriched in serum samples collected during surgery from blood vessels draining directly from lung adenocarcinoma tumor beds. Recently, both miRNAs were found to promote neoangiogenesis in endothelial cells in mouse models of lung adenocarcinoma through targeting of CAMK1D, an inhibitory kinase that can impair angiogenesis when over-expressed. We show that the transfer of miR-143-3p and miR-145-5p within extracellular vesicles from lung adenocarcinoma cells to endothelial cells reduces the levels of CAMK1D and increases tube formation by endothelial cells. This finding suggests that transfer of miRNAs within extracellular vesicles is a method of communication between cancer and endothelial cells which promotes angiogenesis while simultaneously removing tumor suppressive miRNAs within the tumor cells, thus driving tumorigenesis.

Keywords: MiRNA; extracellular vesicles; lung adenocarcinoma; serum miRNA

Conflict of interest statement

CONFLICTS OF INTEREST The authors declare no conflicts of interest.

References

  1. Semin Immunopathol. 2011 Sep;33(5):455-67 - PubMed
  2. Breast Cancer Res. 2016 Sep 08;18(1):90 - PubMed
  3. Nat Rev Genet. 2004 Jul;5(7):522-31 - PubMed
  4. FASEB J. 2014 Jun;28(6):2696-704 - PubMed
  5. Front Genet. 2015 Jan 13;5:472 - PubMed
  6. EMBO J. 2011 Dec 14;30(24):5021 - PubMed
  7. Proteomics. 2014 Mar;14(4-5):412-25 - PubMed
  8. PLoS One. 2014 Dec 04;9(12):e114420 - PubMed
  9. Oncogene. 2014 Feb 27;33(9):1181-9 - PubMed
  10. Oncol Res. 2017 May 24;25(5):651-661 - PubMed
  11. Semin Cell Dev Biol. 2015 Apr;40:41-51 - PubMed
  12. FEBS Lett. 2015 Jun 4;589(13):1391-8 - PubMed
  13. Nat Commun. 2015 Apr 01;6:6716 - PubMed
  14. Nat Commun. 2013;4:2980 - PubMed
  15. J Urol. 2009 Mar;181(3):1372-80 - PubMed
  16. J Cell Mol Med. 2014 Oct;18(10):1913-26 - PubMed
  17. BMC Genomics. 2012 Aug 01;13:357 - PubMed
  18. BMC Clin Pathol. 2014 Jun 21;14:27 - PubMed
  19. Mol Cancer. 2016 Jun 29;15(1):51 - PubMed
  20. Tumour Biol. 2014 Jul;35(7):6235-44 - PubMed
  21. Trends Biochem Sci. 2010 Jul;35(7):368-76 - PubMed
  22. J Biol Chem. 2013 Apr 12;288(15):10849-59 - PubMed
  23. Asian Pac J Cancer Prev. 2014;15(15):6269-73 - PubMed
  24. Oncogene. 2011 Jun 9;30(23 ):2644-58 - PubMed
  25. Cancer Discov. 2016 Feb;6(2):188-201 - PubMed
  26. Genome Biol. 2009;10 (6):R64 - PubMed
  27. Cancer Lett. 2016 Jan 1;370(1):125-35 - PubMed
  28. PLoS One. 2014 Apr 16;9(4):e95240 - PubMed
  29. Angiogenesis. 2012 Mar;15(1):33-45 - PubMed
  30. CA Cancer J Clin. 2011 Jul-Aug;61(4):212-36 - PubMed
  31. Ann Oncol. 2010 May;21 Suppl 5:v103-15 - PubMed
  32. RNA Biol. 2011 Jan-Feb;8(1):125-31 - PubMed
  33. Methods Mol Biol. 2011;784:181-95 - PubMed
  34. Mol Med Rep. 2012 Mar;5(3):753-60 - PubMed
  35. Eur Respir Rev. 2013 Mar 1;22(127):33-6 - PubMed
  36. Oncogene. 2009 Mar 12;28(10 ):1385-92 - PubMed

Publication Types