Mitochondria and Tumor Progression in Ulcerative Colitis
The role of mitochondria in cancer is poorly understood. Ulcerative colitis (UC) is an inflammatory bowel disease that predisposes to colorectal cancer and is an excellent model to study tumor progression. Our goal was to characterize mitochondrial alterations in UC tumorigenesis. Nondysplastic colo...
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| creator | CIGDEM HIMMETOGLU USSAKLI EBAEE, Anoosheh BINKLEY, Jennifer BRENTNALL, Teresa A EMOND, Mary J RABINOVITCH, Peter S RISQUES, Rosa Ana |
| description | The role of mitochondria in cancer is poorly understood. Ulcerative colitis (UC) is an inflammatory bowel disease that predisposes to colorectal cancer and is an excellent model to study tumor progression. Our goal was to characterize mitochondrial alterations in UC tumorigenesis.
Nondysplastic colon biopsies from UC patients with high-grade dysplasia or cancer (progressors; n = 9) and UC patients dysplasia free (nonprogressors; n = 9) were immunostained for cytochrome C oxidase (COX), a component of the electron transport chain, and were quantified by multispectral imaging. For six additional progressors, nondysplastic and dysplastic biopsies were stained for COX and additional mitochondrial proteins including PGC1α, the master regulator of mitochondrial biogenesis. Mitochondrial DNA (mtDNA) copy number was determined by quantitative polymerase chain reaction. Generalized estimating equations with two-sided tests were used to account for correlation of measurements within individuals.
Nondysplastic biopsies of UC progressors showed statistically significant COX loss compared with UC nonprogressors by generalized estimating equation (-18.5 units, 95% confidence interval = -12.1 to -24.9; P < .001). COX intensity progressively decreased with proximity to dysplasia and was the lowest in adjacent to dysplasia and dysplastic epithelium. Surprisingly, COX intensity was statistically significantly increased in cancers. This bimodal pattern was observed for other mitochondrial proteins, including PGC1α, and was confirmed by mtDNA copy number.
Mitochondrial loss precedes the development of dysplasia, and it could be used to detect and potentially predict cancer. Cancer cells restore mitochondria, suggesting that mitochondria are needed for further proliferation. This bimodal pattern might be driven by transcriptional regulation of mitochondrial biogenesis by PGC1α. |
| doi_str_mv | 10.1093/jnci/djt167 |
| format | Article |
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Nondysplastic colon biopsies from UC patients with high-grade dysplasia or cancer (progressors; n = 9) and UC patients dysplasia free (nonprogressors; n = 9) were immunostained for cytochrome C oxidase (COX), a component of the electron transport chain, and were quantified by multispectral imaging. For six additional progressors, nondysplastic and dysplastic biopsies were stained for COX and additional mitochondrial proteins including PGC1α, the master regulator of mitochondrial biogenesis. Mitochondrial DNA (mtDNA) copy number was determined by quantitative polymerase chain reaction. Generalized estimating equations with two-sided tests were used to account for correlation of measurements within individuals.
Nondysplastic biopsies of UC progressors showed statistically significant COX loss compared with UC nonprogressors by generalized estimating equation (-18.5 units, 95% confidence interval = -12.1 to -24.9; P < .001). COX intensity progressively decreased with proximity to dysplasia and was the lowest in adjacent to dysplasia and dysplastic epithelium. Surprisingly, COX intensity was statistically significantly increased in cancers. This bimodal pattern was observed for other mitochondrial proteins, including PGC1α, and was confirmed by mtDNA copy number.
Mitochondrial loss precedes the development of dysplasia, and it could be used to detect and potentially predict cancer. Cancer cells restore mitochondria, suggesting that mitochondria are needed for further proliferation. This bimodal pattern might be driven by transcriptional regulation of mitochondrial biogenesis by PGC1α.</description><identifier>ISSN: 0027-8874</identifier><identifier>EISSN: 1460-2105</identifier><identifier>DOI: 10.1093/jnci/djt167</identifier><identifier>PMID: 23852949</identifier><identifier>CODEN: JNCIEQ</identifier><language>eng</language><publisher>Cary, NC: Oxford University Press</publisher><subject>Adult ; Aged ; Biological and medical sciences ; Biosynthesis ; Cancer ; Case-Control Studies ; Cell Transformation, Neoplastic - metabolism ; Cell Transformation, Neoplastic - pathology ; Colitis, Ulcerative - genetics ; Colitis, Ulcerative - metabolism ; Colitis, Ulcerative - pathology ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Disease Progression ; DNA Copy Number Variations ; Electron Transport Complex IV - genetics ; Electron Transport Complex IV - metabolism ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Glycolysis ; Humans ; Immunohistochemistry ; In Situ Hybridization, Fluorescence ; Inflammatory bowel disease ; Male ; Medical sciences ; Middle Aged ; Mitochondria ; Mitochondria - genetics ; Mitochondria - metabolism ; Mitochondria - ultrastructure ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Polymerase Chain Reaction - methods ; Precancerous Conditions - metabolism ; Precancerous Conditions - pathology ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Telomere Shortening ; Transcription Factors - metabolism ; Tumors</subject><ispartof>JNCI : Journal of the National Cancer Institute, 2013-08, Vol.105 (16), p.1239-1248</ispartof><rights>2014 INIST-CNRS</rights><rights>Copyright Oxford Publishing Limited(England) Aug 21, 2013</rights><rights>The Author 2013. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com. 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c439t-33bfbd16d116376f7291f47cd3dc53bf04bb969f4d32f229aca3a9e9a07de20b3</citedby><cites>FETCH-LOGICAL-c439t-33bfbd16d116376f7291f47cd3dc53bf04bb969f4d32f229aca3a9e9a07de20b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27734847$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23852949$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CIGDEM HIMMETOGLU USSAKLI</creatorcontrib><creatorcontrib>EBAEE, Anoosheh</creatorcontrib><creatorcontrib>BINKLEY, Jennifer</creatorcontrib><creatorcontrib>BRENTNALL, Teresa A</creatorcontrib><creatorcontrib>EMOND, Mary J</creatorcontrib><creatorcontrib>RABINOVITCH, Peter S</creatorcontrib><creatorcontrib>RISQUES, Rosa Ana</creatorcontrib><title>Mitochondria and Tumor Progression in Ulcerative Colitis</title><title>JNCI : Journal of the National Cancer Institute</title><addtitle>J Natl Cancer Inst</addtitle><description>The role of mitochondria in cancer is poorly understood. Ulcerative colitis (UC) is an inflammatory bowel disease that predisposes to colorectal cancer and is an excellent model to study tumor progression. Our goal was to characterize mitochondrial alterations in UC tumorigenesis.
Nondysplastic colon biopsies from UC patients with high-grade dysplasia or cancer (progressors; n = 9) and UC patients dysplasia free (nonprogressors; n = 9) were immunostained for cytochrome C oxidase (COX), a component of the electron transport chain, and were quantified by multispectral imaging. For six additional progressors, nondysplastic and dysplastic biopsies were stained for COX and additional mitochondrial proteins including PGC1α, the master regulator of mitochondrial biogenesis. Mitochondrial DNA (mtDNA) copy number was determined by quantitative polymerase chain reaction. Generalized estimating equations with two-sided tests were used to account for correlation of measurements within individuals.
Nondysplastic biopsies of UC progressors showed statistically significant COX loss compared with UC nonprogressors by generalized estimating equation (-18.5 units, 95% confidence interval = -12.1 to -24.9; P < .001). COX intensity progressively decreased with proximity to dysplasia and was the lowest in adjacent to dysplasia and dysplastic epithelium. Surprisingly, COX intensity was statistically significantly increased in cancers. This bimodal pattern was observed for other mitochondrial proteins, including PGC1α, and was confirmed by mtDNA copy number.
Mitochondrial loss precedes the development of dysplasia, and it could be used to detect and potentially predict cancer. Cancer cells restore mitochondria, suggesting that mitochondria are needed for further proliferation. This bimodal pattern might be driven by transcriptional regulation of mitochondrial biogenesis by PGC1α.</description><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Biosynthesis</subject><subject>Cancer</subject><subject>Case-Control Studies</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Cell Transformation, Neoplastic - pathology</subject><subject>Colitis, Ulcerative - genetics</subject><subject>Colitis, Ulcerative - metabolism</subject><subject>Colitis, Ulcerative - pathology</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Disease Progression</subject><subject>DNA Copy Number Variations</subject><subject>Electron Transport Complex IV - genetics</subject><subject>Electron Transport Complex IV - metabolism</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Glycolysis</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>In Situ Hybridization, Fluorescence</subject><subject>Inflammatory bowel disease</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mitochondria</subject><subject>Mitochondria - genetics</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - ultrastructure</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</subject><subject>Polymerase Chain Reaction - methods</subject><subject>Precancerous Conditions - metabolism</subject><subject>Precancerous Conditions - pathology</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Telomere Shortening</subject><subject>Transcription Factors - metabolism</subject><subject>Tumors</subject><issn>0027-8874</issn><issn>1460-2105</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkE1LAzEQhoMotlZP3mVBPMnafHWzuQhS_IKKHtpzyCbZNmWb1GS34L83pbXqXOYwz7wzPABcIniHICfDpVN2qJctKtgR6CNawBwjODoGfQgxy8uS0R44i3EJU3FMT0EPk3KEOeV9UL7Z1quFdzpYmUmns2m38iH7CH4eTIzWu8y6bNYoE2RrNyYb-8a2Np6Dk1o20Vzs-wDMnh6n45d88v78On6Y5IoS3uaEVHWlUaERKggraoY5qilTmmg1SjNIq4oXvKaa4BpjLpUkkhsuIdMGw4oMwP0ud91VK6OVcW2QjVgHu5LhS3hpxf-Jswsx9xtBGC0hLFLA9T4g-M_OxFYsfRdc-lkgShAqUXKSqNsdpYKPMZj6cAFBsdUstprFTnOir_4-dWB_vCbgZg_IqGRTB5m24y_HGKElZeQbhDGHxA</recordid><startdate>20130821</startdate><enddate>20130821</enddate><creator>CIGDEM HIMMETOGLU USSAKLI</creator><creator>EBAEE, Anoosheh</creator><creator>BINKLEY, Jennifer</creator><creator>BRENTNALL, Teresa A</creator><creator>EMOND, Mary J</creator><creator>RABINOVITCH, Peter S</creator><creator>RISQUES, Rosa Ana</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>5PM</scope></search><sort><creationdate>20130821</creationdate><title>Mitochondria and Tumor Progression in Ulcerative Colitis</title><author>CIGDEM HIMMETOGLU USSAKLI ; EBAEE, Anoosheh ; BINKLEY, Jennifer ; BRENTNALL, Teresa A ; EMOND, Mary J ; RABINOVITCH, Peter S ; RISQUES, Rosa Ana</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c439t-33bfbd16d116376f7291f47cd3dc53bf04bb969f4d32f229aca3a9e9a07de20b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Biosynthesis</topic><topic>Cancer</topic><topic>Case-Control Studies</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Cell Transformation, Neoplastic - pathology</topic><topic>Colitis, Ulcerative - genetics</topic><topic>Colitis, Ulcerative - metabolism</topic><topic>Colitis, Ulcerative - pathology</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Disease Progression</topic><topic>DNA Copy Number Variations</topic><topic>Electron Transport Complex IV - genetics</topic><topic>Electron Transport Complex IV - metabolism</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Glycolysis</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>In Situ Hybridization, Fluorescence</topic><topic>Inflammatory bowel disease</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mitochondria</topic><topic>Mitochondria - genetics</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondria - ultrastructure</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</topic><topic>Polymerase Chain Reaction - methods</topic><topic>Precancerous Conditions - metabolism</topic><topic>Precancerous Conditions - pathology</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. 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Ulcerative colitis (UC) is an inflammatory bowel disease that predisposes to colorectal cancer and is an excellent model to study tumor progression. Our goal was to characterize mitochondrial alterations in UC tumorigenesis.
Nondysplastic colon biopsies from UC patients with high-grade dysplasia or cancer (progressors; n = 9) and UC patients dysplasia free (nonprogressors; n = 9) were immunostained for cytochrome C oxidase (COX), a component of the electron transport chain, and were quantified by multispectral imaging. For six additional progressors, nondysplastic and dysplastic biopsies were stained for COX and additional mitochondrial proteins including PGC1α, the master regulator of mitochondrial biogenesis. Mitochondrial DNA (mtDNA) copy number was determined by quantitative polymerase chain reaction. Generalized estimating equations with two-sided tests were used to account for correlation of measurements within individuals.
Nondysplastic biopsies of UC progressors showed statistically significant COX loss compared with UC nonprogressors by generalized estimating equation (-18.5 units, 95% confidence interval = -12.1 to -24.9; P < .001). COX intensity progressively decreased with proximity to dysplasia and was the lowest in adjacent to dysplasia and dysplastic epithelium. Surprisingly, COX intensity was statistically significantly increased in cancers. This bimodal pattern was observed for other mitochondrial proteins, including PGC1α, and was confirmed by mtDNA copy number.
Mitochondrial loss precedes the development of dysplasia, and it could be used to detect and potentially predict cancer. Cancer cells restore mitochondria, suggesting that mitochondria are needed for further proliferation. This bimodal pattern might be driven by transcriptional regulation of mitochondrial biogenesis by PGC1α.</abstract><cop>Cary, NC</cop><pub>Oxford University Press</pub><pmid>23852949</pmid><doi>10.1093/jnci/djt167</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Biological and medical sciences Biosynthesis Cancer Case-Control Studies Cell Transformation, Neoplastic - metabolism Cell Transformation, Neoplastic - pathology Colitis, Ulcerative - genetics Colitis, Ulcerative - metabolism Colitis, Ulcerative - pathology Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Disease Progression DNA Copy Number Variations Electron Transport Complex IV - genetics Electron Transport Complex IV - metabolism Female Gastroenterology. Liver. Pancreas. Abdomen Glycolysis Humans Immunohistochemistry In Situ Hybridization, Fluorescence Inflammatory bowel disease Male Medical sciences Middle Aged Mitochondria Mitochondria - genetics Mitochondria - metabolism Mitochondria - ultrastructure Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha Polymerase Chain Reaction - methods Precancerous Conditions - metabolism Precancerous Conditions - pathology Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Telomere Shortening Transcription Factors - metabolism Tumors |
| title | Mitochondria and Tumor Progression in Ulcerative Colitis |
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