A novel spontaneous model of epithelial-mesenchymal transition (EMT) using a primary prostate cancer derived cell line demonstrating distinct stem-like characteristics

Harner-Foreman, N, Vadakekolathu, J ORCID: https://orcid.org/0000-0002-2671-4285, Laversin, SA, Mathieu, MG, Reeder, S, Pockley, AG ORCID: https://orcid.org/0000-0001-9593-6431, Rees, RC ORCID: https://orcid.org/0000-0002-4574-4746 and Boocock, DJ ORCID: https://orcid.org/0000-0002-7333-3549, 2017. A novel spontaneous model of epithelial-mesenchymal transition (EMT) using a primary prostate cancer derived cell line demonstrating distinct stem-like characteristics. Scientific Reports, 7, p. 40633. ISSN 2045-2322

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Abstract

Cells acquire the invasive and migratory properties necessary for the invasion-metastasis cascade and the establishment of aggressive, metastatic disease by reactivating a latent embryonic programme: epithelial-to-mesenchymal transition (EMT). Herein, we report the development of a new, spontaneous model of EMT which involves four phenotypically distinct clones derived from a primary tumour-derived human prostate cancer cell line (OPCT-1), and its use to explore relationships between EMT and the generation of cancer stem cells (CSCs) in prostate cancer. Expression of epithelial (E-cadherin) and mesenchymal markers (vimentin, fibronectin) revealed that two of the four clones were incapable of spontaneously activating EMT, whereas the others contained large populations of EMT-derived, vimentin-positive cells having spindle-like morphology. One of the two EMT-positive clones exhibited aggressive and stem cell-like characteristics, whereas the other was non-aggressive and showed no stem cell phenotype. One of the two EMT-negative clones exhibited aggressive stem cell-like properties, whereas the other was the least aggressive of all clones. These findings demonstrate the existence of distinct, aggressive CSC-like populations in prostate cancer, but, importantly, that not all cells having a potential for EMT exhibit stem cell-like properties. This unique model can be used to further interrogate the biology of EMT in prostate cancer.

Item Type:	Journal article
Publication Title:	Scientific Reports
Creators:	Harner-Foreman, N., Vadakekolathu, J., Laversin, S.A., Mathieu, M.G., Reeder, S., Pockley, A.G., Rees, R.C. and Boocock, D.J.
Publisher:	Nature Publishing Group
Date:	17 January 2017
Volume:	7
ISSN:	2045-2322
Identifiers:	Number Type 10.1038/srep40633 DOI
Divisions:	Schools > School of Science and Technology
Record created by:	Jonathan Gallacher
Date Added:	18 Jan 2017 09:02
Last Modified:	04 Feb 2022 16:59
URI:	https://irep.ntu.ac.uk/id/eprint/29798

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