Epithelial Na,K-ATPase expression is down-regulated in canine prostate cancer; a possible consequence of metabolic transformation in the process of prostate malignancy |
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Authors: | Email author" target="_blank">Ali?MobasheriEmail author Richard?Fox Iain?Evans Fay?Cullingham Pablo?Martín-Vasallo Christopher?S?Foster |
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Institution: | Molecular Pathogenesis Research Group, Department of Veterinary Preclinical Sciences, Faculty of Veterinary Science, University of Liverpool, Liverpool L69 7ZJ, United Kingdom. a.mobasheri@liverpool.ac.uk |
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Abstract: | Background An important physiological function of the normal prostate gland is the synthesis and secretion of a citrate rich prostatic
fluid. In prostate cancer, citrate production levels are reduced as a result of altered cellular metabolism and bioenergetics.
Na, K-ATPase is essential for citrate production since the inward Na+ gradients it generates are utilized for the Na+ dependent uptake of aspartate, a major substrate for citrate synthesis. The objective of this study was to compare the expression
of previously identified Na, K-ATPase isoforms in normal canine prostate, benign prostatic hyperplasia (BPH) and prostatic
adenocarcinoma (PCa) using immunohistochemistry in order to determine whether reduced citrate levels in PCa are also accompanied
by changes in Na, K-ATPase expression. |
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