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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/41703
Title: Detachment-induced E-cadherin expression promotes 3D tumor spheroid formation but inhibits tumor formation and metastasis of lung cancer cells
Authors: Phattrakorn Powan
Sudjit Luanpitpong
Xiaoqing He
Yon Rojanasakul
Pithi Chanvorachote
Chulalongkorn University
Mahidol University
West Virginia University
West Virginia University Robert C. Byrd Health Sciences Center
Keywords: Biochemistry, Genetics and Molecular Biology
Issue Date: 7-Nov-2017
Citation: American Journal of Physiology - Cell Physiology. Vol.313, No.5 (2017), C556-C566
Abstract: © 2017 the American Physiological Society. The epithelial-to-mesenchymal transition is proposed to be a key mechanism responsible for metastasis-related deaths. Similarly, cancer stem cells (CSCs) have been proposed to be a key driver of tumor metastasis. However, the link between the two events and their control mechanisms is unclear. We used a three-dimensional (3D) tumor spheroid assay and other CSCindicating assays to investigate the role of E-cadherin in CSC regulation and its association to epithelial-to-mesenchymal transition in lung cancer cells. Ectopic overexpression and knockdown of E-cadherin were found to promote and retard, respectively, the formation of tumor spheroids in vitro but had opposite effects on tumor formation and metastasis in vivo in a xenograft mouse model. We explored the discrepancy between the in vitro and in vivo results and demonstrated, for the first time, that E-cadherin is required as a component of a major survival pathway under detachment conditions. Downregulation of E-cadherin increased the stemness of lung cancer cells but had an adverse effect on their survival, particularly on non-CSCs. Such downregulation also promoted anoikis resistance and invasiveness of lung cancer cells. These results suggest that anoikis assay could be used as an alternative method for in vitro assessment of CSCs that involves dysregulated adhesion proteins. Our data also suggest that agents that restore E-cadherin expression may be used as therapeutic agents for metastatic cancers.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85033452553&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/41703
ISSN: 15221563
03636143
Appears in Collections:Scopus 2016-2017

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