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Tumor Biology
Published in: Tumor Biology 12/2015

01-12-2015 | Research Article

Extracellular vesicles from women with breast cancer promote an epithelial-mesenchymal transition-like process in mammary epithelial cells MCF10A

Authors: Octavio Galindo-Hernandez, Cristina Gonzales-Vazquez, Pedro Cortes-Reynosa, Emmanuel Reyes-Uribe, Sonia Chavez-Ocaña, Octavio Reyes-Hernandez, Mónica Sierra-Martinez, Eduardo Perez Salazar

Published in: Tumor Biology | Issue 12/2015

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Abstract

Extracellular vesicles (EVs) mediate many stages of tumor progression including angiogenesis, escape from immune surveillance, and extracellular matrix degradation. We studied whether EVs from plasma of women with breast cancer are able to induce an epithelial-mesenchymal transition (EMT) process in mammary epithelial cells MCF10A. Our findings demonstrate that EVs from plasma of breast cancer patients induce a downregulation of E-cadherin expression and an increase of vimentin and N-cadherin expression. Moreover, EVs induce migration and invasion, as well as an increase of NFκB-DNA binding activity and MMP-2 and MMP-9 secretions. In summary, our findings demonstrate, for the first time, that EVs from breast cancer patients induce an EMT-like process in human mammary non-tumorigenic epithelial cells MCF10A.
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Literature
1.
Al-Nedawi K, Meehan B, Rak J. Microvesicles: messengers and mediators of tumor progression. Cell Cycle. 2009;8:2014–8.CrossRefPubMed
2.
3.
4.
Muralidharan-Chari V, Clancy JW, Sedgwick A, D'Souza-Schorey C. Microvesicles. Mediators of extracellular communication during cancer progression. J Cell Sci. 2010;123:1603–11.CrossRefPubMedPubMedCentral
5.
6.
Jy W, Horstman LL, Jimenez JJ, Ahn YS, Biro E, Nieuwland R, et al. Measuring circulating cell-derived microparticles. J Thromb Haemost. 2004;2:1842–51.CrossRefPubMed
7.
Thery C, Zitvogel L, Amigorena S. Exosomes. Composition, biogenesis and function. Nat Rev Immunol. 2002;2:569–79.PubMed
8.
Baran J, Baj-Krzyworzeka M, Weglarczyk K, Szatanek R, Zembala M, Barbasz J, et al. Circulating tumour-derived microvesicles in plasma of gastric cancer patients. Cancer Immunol Immunother. 2010;59:841–50.CrossRefPubMed
9.
Kim HK, Song KS, Park YS, Kang YH, Lee YJ, Lee KR, et al. Elevated levels of circulating platelet microparticles, VEGF, IL-6 and RANTES in patients with gastric cancer: Possible role of a metastasis predictor. Eur J Cancer. 2003;39:184–91.CrossRefPubMed
10.
Galindo-Hernandez O, Villegas-Comonfort S, Candanedo F, Gonzalez-Vazquez MC, Chavez-Ocana S, Jimenez-Villanueva X, et al. Elevated concentration of microvesicles isolated from peripheral blood in breast cancer patients. Arch Med Res. 2013;44:208–14.CrossRefPubMed
11.
Kong D, Li Y, Wang Z, Sarkar FH. Cancer stem cells and epithelial-to-mesenchymal transition (EMT)-phenotypic cells: are they cousins or twins? Cancers (Basel). 2011;3:716–29.CrossRef
12.
Kawamoto T, Ohga N, Akiyama K, Hirata N, Kitahara S, Maishi N, et al. Tumor-derived microvesicles induce proangiogenic phenotype in endothelial cells via endocytosis. PLoS One. 2012;7, e34045.CrossRefPubMedPubMedCentral
13.
Espinosa-Neira R, Mejia-Rangel J, Cortes-Reynosa P, Salazar EP. Linoleic acid induces an EMT-like process in mammary epithelial cells MCF10a. Int J Biochem Cell Biol. 2011;43:1782–91.CrossRefPubMed
14.
15.
16.
Antonyak MA, Li B, Boroughs LK, Johnson JL, Druso JE, Bryant KL, et al. Cancer cell-derived microvesicles induce transformation by transferring tissue transglutaminase and fibronectin to recipient cells. Proc Natl Acad Sci U S A. 2011;108:4852–7.CrossRefPubMedPubMedCentral
17.
Lee JM, Dedhar S, Kalluri R, Thompson EW. The epithelial-mesenchymal transition: new insights in signaling, development, and disease. J Cell Biol. 2006;172:973–81.CrossRefPubMedPubMedCentral
18.
Skog J, Wurdinger T, van Rijn S, Meijer DH, Gainche L, Sena-Esteves M, et al. Glioblastoma microvesicles transport RNA and proteins that promote tumour growth and provide diagnostic biomarkers. Nat Cell Biol. 2008;10:1470–6.CrossRefPubMedPubMedCentral
19.
Gavert N, Ben-Ze'ev A. Epithelial-mesenchymal transition and the invasive potential of tumors. Trends Mol Med. 2008;14:199–209.CrossRefPubMed
20.
Hajra KM, Chen DY, Fearon ER. The slug zinc-finger protein represses e-cadherin in breast cancer. Cancer Res. 2002;62:1613–8.PubMed
21.
Eger A, Aigner K, Sonderegger S, Dampier B, Oehler S, Schreiber M, et al. Deltaef1 is a transcriptional repressor of e-cadherin and regulates epithelial plasticity in breast cancer cells. Oncogene. 2005;24:2375–85.CrossRefPubMed
22.
Dong R, Wang Q, He XL, Chu YK, Lu JG, Ma QJ. Role of nuclear factor kappa b and reactive oxygen species in the tumor necrosis factor-alpha-induced epithelial-mesenchymal transition of mcf-7 cells. Braz J Med Biol Res. 2007;40:1071–8.CrossRefPubMed
23.
Huber MA, Azoitei N, Baumann B, Grunert S, Sommer A, Pehamberger H, et al. Nf-kappab is essential for epithelial-mesenchymal transition and metastasis in a model of breast cancer progression. J Clin Invest. 2004;114:569–81.CrossRefPubMedPubMedCentral
24.
25.
26.
D'Souza-Schorey C, Clancy JW. Tumor-derived microvesicles: shedding light on novel microenvironment modulators and prospective cancer biomarkers. Genes Dev. 2012;26:1287–99.CrossRefPubMedPubMedCentral
27.
Gumbiner BM. Regulation of cadherin-mediated adhesion in morphogenesis. Nat Rev Mol Cell Biol. 2005;6:622–34.CrossRefPubMed
28.
Thiery JP. Epithelial-mesenchymal transitions in development and pathologies. Curr Opin Cell Biol. 2003;15:740–6.CrossRefPubMed
29.
Cano A, Perez-Moreno MA, Rodrigo I, Locascio A, Blanco MJ, del Barrio MG, et al. The transcription factor snail controls epithelial-mesenchymal transitions by repressing e-cadherin expression. Nat Cell Biol. 2000;2:76–83.CrossRefPubMed
30.
31.
Diamant M, Nieuwland R, Pablo RF, Sturk A, Smit JW, Radder JK. Elevated numbers of tissue-factor exposing microparticles correlate with components of the metabolic syndrome in uncomplicated type 2 diabetes mellitus. Circulation. 2002;106:2442–7.CrossRefPubMed
32.
Hazan RB, Phillips GR, Qiao RF, Norton L, Aaronson SA. Exogenous expression of n-cadherin in breast cancer cells induces cell migration, invasion, and metastasis. J Cell Biol. 2000;148:779–90.CrossRefPubMedPubMedCentral
33.
Bindels S, Mestdagt M, Vandewalle C, Jacobs N, Volders L, Noel A, et al. Regulation of vimentin by sip1 in human epithelial breast tumor cells. Oncogene. 2006;25:4975–85.CrossRefPubMed
34.
Min C, Eddy SF, Sherr DH, Sonenshein GE. Nf-kappab and epithelial to mesenchymal transition of cancer. J Cell Biochem. 2008;104:733–44.CrossRefPubMed
35.
Radisky ES, Radisky DC. Matrix metalloproteinase-induced epithelial-mesenchymal transition in breast cancer. J Mammary Gland Biol Neoplasia. 2010;15:201–12.CrossRefPubMedPubMedCentral
36.
Radenkovic S, Konjevic G, Jurisic V, Karadzic K, Nikitovic M, Gopcevic K. Values of mmp-2 and mmp-9 in tumor tissue of basal-like breast cancer patients. Cell Biochem Biophys. 2014;68:143–52.CrossRefPubMed
37.
38.
39.
40.
Turturici G, Tinnirello R, Sconzo G, Geraci F. Extracellular membrane vesicles as a mechanism of cell-to-cell communication: advantages and disadvantages. Am J Physiol Cell Physiol. 2014;306:C621–33.CrossRefPubMed
Metadata
Title
Extracellular vesicles from women with breast cancer promote an epithelial-mesenchymal transition-like process in mammary epithelial cells MCF10A
Authors
Octavio Galindo-Hernandez
Cristina Gonzales-Vazquez
Pedro Cortes-Reynosa
Emmanuel Reyes-Uribe
Sonia Chavez-Ocaña
Octavio Reyes-Hernandez
Mónica Sierra-Martinez
Eduardo Perez Salazar
Publication date
01-12-2015
Publisher
Springer Netherlands
Published in
Tumor Biology / Issue 12/2015
Print ISSN: 1010-4283
Electronic ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-015-3711-9

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