Research Papers: Pathology:
Altered expression of epithelial-to-mesenchymal transition proteins in extraprostatic prostate cancer
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Clare Verrill1,2, Lucia Cerundolo2, Chad Mckee3, Michael White4, Christiana Kartsonaki5, Eve Fryer1, Emma Morris2,4, Simon Brewster6, Indrika Ratnayaka4, Luke Marsden2, Hans Lilja2,7,8,9, Ruth Muschel3, Xin Lu4, Freddie Hamdy2 and Richard J. Bryant2,4
1 Department of Cellular Pathology, Oxford University Hospitals NHS Foundation Trust, John Radcliffe Hospital, Headington, Oxford, UK
2 Nuffield Department of Surgical Sciences, University of Oxford, Headington, Oxford, UK
3 CRUK/MRC Oxford Institute for Radiation Oncology, University of Oxford, Headington, Oxford, UK
4 Ludwig Institute for Cancer Research Ltd, University of Oxford, Nuffield Department of Clinical Medicine, Headington, Oxford, UK
5 Department of Oncology, University of Oxford, Headington, Oxford, UK
6 Department of Urology, Churchill Hospital, Headington, Oxford, UK
7 Departments of Surgery (Urology Service), Laboratory Medicine (Clinical Chemistry Service) and Medicine (Genitourinary Oncology Service), Memorial Sloan Kettering Cancer Center, New York, NY, USA
8 Department of Laboratory Medicine and Clinical Sciences in Malmö, Lund University, Skåne University Hospital, Malmö, Sweden
9 Institute of Biomedical Technology, University of Tampere, Tampere, Finland
Richard J. Bryant, email:
Keywords: epithelial to mesenchymal transition, extraprostatic prostate cancer, immunohistochemistry, in vitro organotypic cell culture, in vivo mouse prostate cancer model, Pathology Section
Received: July 15, 2015 Accepted: December 05, 2015 Published: January 12, 2016
Epithelial to mesenchymal transition (EMT) of cancer cells involves loss of epithelial polarity and adhesiveness, and gain of invasive and migratory mesenchymal behaviours. EMT occurs in prostate cancer (PCa) but it is unknown whether this is in specific areas of primary tumours. We examined whether any of eleven EMT-related proteins have altered expression or subcellular localisation within the extraprostatic extension component of locally advanced PCa compared with other localisations, and whether similar changes may occur in in vitro organotypic PCa cell cultures and in vivo PCa models. Expression profiles of three proteins (E-cadherin, Snail, and α-smooth muscle actin) were significantly different in extraprostatic extension PCa compared with intra-prostatic tumour, and 18/27 cases had an expression change of at least one of these three proteins. Of the three significantly altered EMT proteins in pT3 samples, one showed similar significantly altered expression patterns in in vitro organotypic culture models, and two in in vivo Pten-/- model samples. These results suggest that changes in EMT protein expression can be observed in the extraprostatic extension component of locally invasive PCa. The biology of some of these changes in protein expression may be studied in certain in vitro and in vivo PCa models.
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