Extracellular Vesicles Released from Cancer Cells Promote Tumorigenesis by Inducing Epithelial to Mesenchymal Transition via β-Catenin Signaling

Malyla, V; Paudel, KR; Rubis, GD; Hansbro, NG; Hansbro, PM; Dua, K

Extracellular Vesicles Released from Cancer Cells Promote Tumorigenesis by Inducing Epithelial to Mesenchymal Transition via β-Catenin Signaling

Malyla, V Paudel, KR Rubis, GD Hansbro, NG Hansbro, PM Dua, K

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Publisher:: MDPI AG
Publication Type:: Journal Article
Citation:: International Journal of Molecular Sciences, 24, (4), pp. 3500-3500

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Field	Value	Language
dc.contributor.author	Malyla, V
dc.contributor.author	Paudel, KR
dc.contributor.author	Rubis, GD
dc.contributor.author	Hansbro, NG
dc.contributor.author	Hansbro, PM
dc.contributor.author	Dua, K
dc.date.accessioned	2023-02-12T11:18:19Z
dc.date.available	2023-02-12T11:18:19Z
dc.identifier.citation	International Journal of Molecular Sciences, 24, (4), pp. 3500-3500
dc.identifier.issn	1422-0067
dc.identifier.uri	http://hdl.handle.net/10453/166059
dc.description.abstract	<jats:p>Lung cancer is the leading cause of cancer-related deaths globally, in part due to a lack of early diagnostic tools and effective pharmacological interventions. Extracellular vesicles (EVs) are lipid-based membrane-bound particles released from all living cells in both physiological and pathological states. To understand the effects of lung-cancer-derived EVs on healthy cells, we isolated and characterized EVs derived from A549 lung adenocarcinoma cells and transferred them to healthy human bronchial epithelial cells (16HBe14o). We found that A549-derived EVs carry oncogenic proteins involved in the pathway of epithelial to mesenchymal transition (EMT) that are regulated by β-catenin. The exposure of 16HBe14o cells to A549-derived EVs resulted in a significant increase in cell proliferation, migration, and invasion via upregulating EMT markers such as E-Cadherin, Snail, and Vimentin and cell adhesion molecules such as CEACAM-5, ICAM-1, and VCAM-1, with concomitant downregulation of EpCAM. Our study suggests a role for cancer-cell-derived EVs to induce tumorigenesis in adjacent healthy cells by promoting EMT via β-catenin signaling.</jats:p>
dc.language	en
dc.publisher	MDPI AG
dc.relation	International Association for the Study of Lung Cancer Foundation
dc.relation.ispartof	International Journal of Molecular Sciences
dc.relation.isbasedon	10.3390/ijms24043500
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	0399 Other Chemical Sciences, 0604 Genetics, 0699 Other Biological Sciences
dc.subject.classification	Chemical Physics
dc.title	Extracellular Vesicles Released from Cancer Cells Promote Tumorigenesis by Inducing Epithelial to Mesenchymal Transition via β-Catenin Signaling
dc.type	Journal Article
utslib.citation.volume	24
utslib.for	0399 Other Chemical Sciences
utslib.for	0604 Genetics
utslib.for	0699 Other Biological Sciences
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Strength - CFI - Centre for Inflammation
utslib.copyright.status	open_access	*
dc.date.updated	2023-02-12T11:18:13Z
pubs.issue	4
pubs.publication-status	Published online
pubs.volume	24
utslib.citation.issue	4

Abstract:

Lung cancer is the leading cause of cancer-related deaths globally, in part due to a lack of early diagnostic tools and effective pharmacological interventions. Extracellular vesicles (EVs) are lipid-based membrane-bound particles released from all living cells in both physiological and pathological states. To understand the effects of lung-cancer-derived EVs on healthy cells, we isolated and characterized EVs derived from A549 lung adenocarcinoma cells and transferred them to healthy human bronchial epithelial cells (16HBe14o). We found that A549-derived EVs carry oncogenic proteins involved in the pathway of epithelial to mesenchymal transition (EMT) that are regulated by β-catenin. The exposure of 16HBe14o cells to A549-derived EVs resulted in a significant increase in cell proliferation, migration, and invasion via upregulating EMT markers such as E-Cadherin, Snail, and Vimentin and cell adhesion molecules such as CEACAM-5, ICAM-1, and VCAM-1, with concomitant downregulation of EpCAM. Our study suggests a role for cancer-cell-derived EVs to induce tumorigenesis in adjacent healthy cells by promoting EMT via β-catenin signaling.

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http://hdl.handle.net/10453/166059