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Sci Rep ; 7: 40633, 2017 01 17.
Article in English | MEDLINE | ID: mdl-28094783

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.


Subject(s)
Epithelial-Mesenchymal Transition , Neoplastic Stem Cells/metabolism , Prostatic Neoplasms/metabolism , Prostatic Neoplasms/pathology , Biomarkers , Cadherins/metabolism , Cell Line, Tumor , Cell Movement/genetics , Cell Proliferation , Cell Transformation, Neoplastic/genetics , Drug Resistance, Neoplasm , Epithelial-Mesenchymal Transition/drug effects , Epithelial-Mesenchymal Transition/genetics , Gene Expression Profiling , Gene Expression Regulation, Neoplastic , Humans , Male , Neoplastic Stem Cells/drug effects , Neoplastic Stem Cells/pathology , Prostatic Neoplasms/genetics , Transcriptome , Vimentin/metabolism
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