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Elevated Oestrogen Receptor Splice Variant ERαΔ5 Expression in Tumour-adjacent Hormone-responsive Tissue

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...

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Autores principales: Taylor, Siân E., Patel, Imran I., Singh, Paras B., Nicholson, Caroline M., Stringfellow, Helen F., Gopala Krishna, R. K., Matanhelia, Shyam S., Martin-Hirsch, Pierre L., Martin, Francis L.
Formato: Texto
Lenguaje:English
Publicado: Molecular Diversity Preservation International (MDPI) 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2996214/
https://www.ncbi.nlm.nih.gov/pubmed/21139866
http://dx.doi.org/10.3390/ijerph7113871
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author Taylor, Siân E.
Patel, Imran I.
Singh, Paras B.
Nicholson, Caroline M.
Stringfellow, Helen F.
Gopala Krishna, R. K.
Matanhelia, Shyam S.
Martin-Hirsch, Pierre L.
Martin, Francis L.
author_facet Taylor, Siân E.
Patel, Imran I.
Singh, Paras B.
Nicholson, Caroline M.
Stringfellow, Helen F.
Gopala Krishna, R. K.
Matanhelia, Shyam S.
Martin-Hirsch, Pierre L.
Martin, Francis L.
author_sort Taylor, Siân E.
collection PubMed
description 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 (ERαΔ3, ERαΔ5, ERβ2 and ERβ5), plus the full-length parent isoforms ERα and ERβ1, 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 ERαΔ5. This splice variant was markedly raised in all of the tumour-adjacent prostate samples compared to benign tissues. Immunofluorescence analysis for ERβ2 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 ERαΔ5 may be involved in progression of prostate adenocarcinoma.
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spelling pubmed-29962142010-12-06 Elevated Oestrogen Receptor Splice Variant ERαΔ5 Expression in Tumour-adjacent Hormone-responsive Tissue Taylor, Siân E. Patel, Imran I. Singh, Paras B. Nicholson, Caroline M. Stringfellow, Helen F. Gopala Krishna, R. K. Matanhelia, Shyam S. Martin-Hirsch, Pierre L. Martin, Francis L. Int J Environ Res Public Health Article 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 (ERαΔ3, ERαΔ5, ERβ2 and ERβ5), plus the full-length parent isoforms ERα and ERβ1, 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 ERαΔ5. This splice variant was markedly raised in all of the tumour-adjacent prostate samples compared to benign tissues. Immunofluorescence analysis for ERβ2 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 ERαΔ5 may be involved in progression of prostate adenocarcinoma. Molecular Diversity Preservation International (MDPI) 2010-11 2010-11-02 /pmc/articles/PMC2996214/ /pubmed/21139866 http://dx.doi.org/10.3390/ijerph7113871 Text en © 2010 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0 This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Article
Taylor, Siân E.
Patel, Imran I.
Singh, Paras B.
Nicholson, Caroline M.
Stringfellow, Helen F.
Gopala Krishna, R. K.
Matanhelia, Shyam S.
Martin-Hirsch, Pierre L.
Martin, Francis L.
Elevated Oestrogen Receptor Splice Variant ERαΔ5 Expression in Tumour-adjacent Hormone-responsive Tissue
title Elevated Oestrogen Receptor Splice Variant ERαΔ5 Expression in Tumour-adjacent Hormone-responsive Tissue
title_full Elevated Oestrogen Receptor Splice Variant ERαΔ5 Expression in Tumour-adjacent Hormone-responsive Tissue
title_fullStr Elevated Oestrogen Receptor Splice Variant ERαΔ5 Expression in Tumour-adjacent Hormone-responsive Tissue
title_full_unstemmed Elevated Oestrogen Receptor Splice Variant ERαΔ5 Expression in Tumour-adjacent Hormone-responsive Tissue
title_short Elevated Oestrogen Receptor Splice Variant ERαΔ5 Expression in Tumour-adjacent Hormone-responsive Tissue
title_sort elevated oestrogen receptor splice variant erαδ5 expression in tumour-adjacent hormone-responsive tissue
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2996214/
https://www.ncbi.nlm.nih.gov/pubmed/21139866
http://dx.doi.org/10.3390/ijerph7113871
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