Differential expression of microRNAs in tumors from chronically inflamed or genetic (APC(Min/+)) models of colon cancer.

<h4>Background</h4>Chronic inflammation associated with ulcerative colitis predisposes individuals to increased colon cancer risk. The aim of these studies was to identify microRNAs that are aberrantly regulated during inflammation and may participate in transformation of colonic epithel...

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Autores principales:	Brian M Necela, Jennifer M Carr, Yan W Asmann, E Aubrey Thompson
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/7f476c970436489792dc4094ee5262a9
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spelling	oai:doaj.org-article:7f476c970436489792dc4094ee5262a92021-11-18T06:55:55ZDifferential expression of microRNAs in tumors from chronically inflamed or genetic (APC(Min/+)) models of colon cancer.1932-620310.1371/journal.pone.0018501https://doaj.org/article/7f476c970436489792dc4094ee5262a92011-04-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21532750/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Chronic inflammation associated with ulcerative colitis predisposes individuals to increased colon cancer risk. The aim of these studies was to identify microRNAs that are aberrantly regulated during inflammation and may participate in transformation of colonic epithelial cells in the inflammatory setting.<h4>Methodology/principal findings</h4>We have use quantitative PCR arrays to compare microRNA (miRNA) expression in tumors and control colonic epithelial cells isolated from distal colons of chronically inflamed mice and APC(Min/+) mice. Rank order statistics was utilized to identify differentially regulated miRNAs in tumors that arose due to chronic inflammation and/or to germline APC mutation. Eight high priority miRNAs were identified: miR-215, miR-137, miR-708, miR-31, and miR-135b were differentially expressed in APC tumors and miR-215, miR-133a, miR-467d, miR-218, miR-708, miR-31, and miR-135b in colitis-associated tumors. Four of these (miR-215, miR-708, miR-31, and miR-135b) were common to both tumors types, and dysregulation of these miRNAs was confirmed in an independent sample set. Target prediction and pathway analysis suggests that these microRNAs, in the aggregate, regulate signaling pathways related to MAPK, PI3K, WNT, and TGF-β, all of which are known to be involved in transformation.<h4>Conclusions/significance</h4>We conclude that these four miRNAs are dysregulated at some very early stage in transformation of colonic epithelial cells. This response is not dependent on the mechanism of initiation of transformation (inflammation versus germline mutation), suggesting that the miRNAs that we have identified are likely to regulate critical signaling pathways that are central to early events in transformation of colonic epithelial cells.Brian M NecelaJennifer M CarrYan W AsmannE Aubrey ThompsonPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 4, p e18501 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Brian M Necela Jennifer M Carr Yan W Asmann E Aubrey Thompson Differential expression of microRNAs in tumors from chronically inflamed or genetic (APC(Min/+)) models of colon cancer.
description	<h4>Background</h4>Chronic inflammation associated with ulcerative colitis predisposes individuals to increased colon cancer risk. The aim of these studies was to identify microRNAs that are aberrantly regulated during inflammation and may participate in transformation of colonic epithelial cells in the inflammatory setting.<h4>Methodology/principal findings</h4>We have use quantitative PCR arrays to compare microRNA (miRNA) expression in tumors and control colonic epithelial cells isolated from distal colons of chronically inflamed mice and APC(Min/+) mice. Rank order statistics was utilized to identify differentially regulated miRNAs in tumors that arose due to chronic inflammation and/or to germline APC mutation. Eight high priority miRNAs were identified: miR-215, miR-137, miR-708, miR-31, and miR-135b were differentially expressed in APC tumors and miR-215, miR-133a, miR-467d, miR-218, miR-708, miR-31, and miR-135b in colitis-associated tumors. Four of these (miR-215, miR-708, miR-31, and miR-135b) were common to both tumors types, and dysregulation of these miRNAs was confirmed in an independent sample set. Target prediction and pathway analysis suggests that these microRNAs, in the aggregate, regulate signaling pathways related to MAPK, PI3K, WNT, and TGF-β, all of which are known to be involved in transformation.<h4>Conclusions/significance</h4>We conclude that these four miRNAs are dysregulated at some very early stage in transformation of colonic epithelial cells. This response is not dependent on the mechanism of initiation of transformation (inflammation versus germline mutation), suggesting that the miRNAs that we have identified are likely to regulate critical signaling pathways that are central to early events in transformation of colonic epithelial cells.
format	article
author	Brian M Necela Jennifer M Carr Yan W Asmann E Aubrey Thompson
author_facet	Brian M Necela Jennifer M Carr Yan W Asmann E Aubrey Thompson
author_sort	Brian M Necela
title	Differential expression of microRNAs in tumors from chronically inflamed or genetic (APC(Min/+)) models of colon cancer.
title_short	Differential expression of microRNAs in tumors from chronically inflamed or genetic (APC(Min/+)) models of colon cancer.
title_full	Differential expression of microRNAs in tumors from chronically inflamed or genetic (APC(Min/+)) models of colon cancer.
title_fullStr	Differential expression of microRNAs in tumors from chronically inflamed or genetic (APC(Min/+)) models of colon cancer.
title_full_unstemmed	Differential expression of microRNAs in tumors from chronically inflamed or genetic (APC(Min/+)) models of colon cancer.
title_sort	differential expression of micrornas in tumors from chronically inflamed or genetic (apc(min/+)) models of colon cancer.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/7f476c970436489792dc4094ee5262a9
work_keys_str_mv	AT brianmnecela differentialexpressionofmicrornasintumorsfromchronicallyinflamedorgeneticapcminmodelsofcoloncancer AT jennifermcarr differentialexpressionofmicrornasintumorsfromchronicallyinflamedorgeneticapcminmodelsofcoloncancer AT yanwasmann differentialexpressionofmicrornasintumorsfromchronicallyinflamedorgeneticapcminmodelsofcoloncancer AT eaubreythompson differentialexpressionofmicrornasintumorsfromchronicallyinflamedorgeneticapcminmodelsofcoloncancer
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Differential expression of microRNAs in tumors from chronically inflamed or genetic (APC(Min/+)) models of colon cancer.

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