%0 Journal Article
%T Elevated Oestrogen Receptor Splice Variant ER¦Á¦¤5 Expression in Tumour-adjacent Hormone-responsive Tissue
%A Sian E. Taylor
%A Imran I. Patel
%A Paras B. Singh
%A Caroline M. Nicholson
%A Helen F. Stringfellow
%A R. K. Gopala Krishna
%A Shyam S. Matanhelia
%A Pierre L. Martin-Hirsch
%A Francis L. Martin
%J International Journal of Environmental Research and Public Health
%D 2010
%I MDPI AG
%R 10.3390/ijerph7113871
%X Susceptibility to prostate or endometrial cancer is linked with obesity, a state of oestrogen excess. Oestrogen receptor (ER) splice variants may be responsible for the tissue-level of ER activity. Such micro-environmental regulation may modulate cancer initiation and/or progression mechanisms. Real-time reverse transcriptase (RT) polymerase chain reaction (PCR) was used to quantitatively assess the levels of four ER splice variants ( ER ¦Á ¦¤ 3, ER ¦Á ¦¤ 5, ER ¦Â2 and ER ¦Â 5), plus the full-length parent isoforms ER ¦Á and ER ¦Â 1, in high-risk [tumour-adjacent prostate ( n = 10) or endometrial cancer ( n = 9)] vs. low-risk [benign prostate ( n = 12) or endometrium ( n = 9)], as well as a comparison of UK ( n = 12) vs. Indian ( n = 15) benign prostate. All three tissue groups expressed the ER splice variants at similar levels, apart from ER ¦Á ¦¤ 5. This splice variant was markedly raised in all of the tumour-adjacent prostate samples compared to benign tissues. Immunofluorescence analysis for ER ¦Â2 in prostate tissue demonstrated that such splice variants are present in comparable, if not greater, amounts as the parent full-length isoform. This small pilot study demonstrates the ubiquitous nature of ER splice variants in these tissue sites and suggests that ER ¦Á ¦¤5 may be involved in progression of prostate adenocarcinoma.
%K endometrial cancer
%K oestrogen receptor
%K prostate cancer
%K real-time RT PCR
%K splice variant
%U http://www.mdpi.com/1660-4601/7/11/3871