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The effect of lithocholic acid on proliferation and apoptosis during the early stages of colon carcinogenesis: differential effect on apoptosis in the presence of a colon carcinogen

The effect of lithocholic acid on proliferation and apoptosis during the early stages of colon... Lithocholic acid (LCA) is implicated in human and experimental animal carcinogenesis. Its effect on apoptosis and proliferation of the colonic epithelium was studied in a 1,2-dimethylhydrazine (DMH)-induced murine carcinogenesis model. Four groups of mice, control, LCA, DMH and DMH+LCA, were studied for 4 weeks, a period corresponding to early stages of carcinogenesis. Apoptosis (AI) and proliferation (PI) indices in the colon were determined by immunohistochemistry. LCA stimulated apoptosis (AI = 1.2 ± 0.3% (all values are the mean ± SEM) versus control 0.5 ± 0.1%, P < 0.05), as did DMH (4.3 ± 0.8%, P < 0.02). DMH increased apoptosis at the base of the crypt nearly 50-fold, with no effect at the lumenal third. In mice receiving DMH, LCA suppressed apoptosis almost completely (0.1 ± 0.03%); this suppression was complete at the lower two-thirds of the crypt (AI = 0) and 60% at the lumenal third. LCA increased proliferation (PI = 22.2 ± 4.6% versus 15.4 ± 1% in controls), but this did not reach statistical significance. DMH increased proliferation (PI = 34.6 ± 2.3%, P < 0.01). In mice receiving DMH, proliferation (41 ± 2.9%) was about two-thirds of the additive effect. LCA affected proliferation, mainly in the middle third of the crypt; DMH's effect was similar in distribution, but more pronounced. In mice receiving DMH, LCA shifts proliferation upward, extending it to the lumenal third of the crypt. LCA's main cell kinetic effect in the colon is on apoptosis; this effect differs in normal (stimulation) and pre-malignant colon (nearly complete suppression). LCA does not significantly stimulate proliferation in either normal or pre-malignant colon. The differential effect of LCA on apoptosis in the presence of a carcinogen partially explains its effect as a promoter on colon carcinogenesis in animal models, and may have important implications for human carcinogenesis. Key words AI, apoptosis index DMH, 1,2-dimethylhydrazine LCA, lithocholic acid PCNA, proliferating cell nuclear antigen PI, proliferation index RT, room temperature TUNEL, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling. © Oxford University Press « Previous | Next Article » Table of Contents This Article Carcinogenesis (2000) 21 (5): 999-1005. doi: 10.1093/carcin/21.5.999 » Abstract Free Full Text (HTML) Free Full Text (PDF) Free Classifications Carcinogenesis Services Article metrics Alert me when cited Alert me if corrected Find similar articles Similar articles in Web of Science Similar articles in PubMed Add to my archive Download citation Request Permissions Citing Articles Load citing article information Citing articles via CrossRef Citing articles via Scopus Citing articles via Web of Science Citing articles via Google Scholar Google Scholar Articles by Kozoni, V. Articles by Rigas, B. Search for related content PubMed PubMed citation Articles by Kozoni, V. Articles by Tsioulias, G. Articles by Shiff, S. Articles by Rigas, B. Related Content Load related web page information Share Email this article CiteULike Delicious Facebook Google+ Mendeley Twitter What's this? Search this journal: Advanced » Current Issue October 2015 36 (10) Alert me to new issues The Journal About this journal Rights & Permissions Dispatch date of the next issue This journal is a member of the Committee on Publication Ethics (COPE) We are mobile – find out more Journals Career Network Impact factor: 5.334 5-Yr impact factor: 5.698 Editor-in-Chief Dr Curtis C Harris, USA View full editorial board For Authors Instructions to authors Online submission Submit Now! Self archiving policy Open access options for authors - visit Oxford Open This journal enables compliance with the NIH Public Access Policy Alerting Services Email table of contents Email Advance Access CiteTrack XML RSS feed Corporate Services Advertising sales Reprints Supplements var taxonomies = ("MED00710"); Most Most Read Apoptosis in cancer Modulation of E-cadherin expression by K-Ras; involvement of DNA methyltransferase-3b Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead Tumor progression and metastasis Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability » View all Most Read articles Most Cited Oxyradicals and DNA damage Sensing and repairing DNA double-strand breaks Functional role of estrogen metabolism in target cells: review and perspectives Apoptosis in cancer Nucleotide excision repair and human syndromes » View all Most Cited articles Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department. Online ISSN 1460-2180 - Print ISSN 0143-3334 Copyright © 2015 Oxford University Press Oxford Journals Oxford University Press Site Map Privacy Policy Cookie Policy Legal Notices Frequently Asked Questions Other Oxford University Press sites: Oxford University Press Oxford Journals China Oxford Journals Japan Academic & Professional books Children's & Schools Books Dictionaries & Reference Dictionary of National Biography Digital Reference English Language Teaching Higher Education Textbooks International Education Unit Law Medicine Music Online Products & Publishing Oxford Bibliographies Online Oxford Dictionaries Online Oxford English Dictionary Oxford Language Dictionaries Online Oxford Scholarship Online Reference Rights and Permissions Resources for Retailers & Wholesalers Resources for the Healthcare Industry Very Short Introductions World's Classics function fnc_onDomLoaded() { var query_context = getQueryContext(); PF_initOIUnderbar(query_context,":QS:default","","JRN"); PF_insertOIUnderbar(0); }; if (window.addEventListener) { window.addEventListener('load', fnc_onDomLoaded, false); } else if (window.attachEvent) { window.attachEvent('onload', fnc_onDomLoaded); } var gaJsHost = (("https:" == document.location.protocol) ? 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The effect of lithocholic acid on proliferation and apoptosis during the early stages of colon carcinogenesis: differential effect on apoptosis in the presence of a colon carcinogen

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References (38)

Publisher
Oxford University Press
Copyright
Copyright © 2015 Oxford University Press
ISSN
0143-3334
eISSN
1460-2180
DOI
10.1093/carcin/21.5.999
Publisher site
See Article on Publisher Site

Abstract

Lithocholic acid (LCA) is implicated in human and experimental animal carcinogenesis. Its effect on apoptosis and proliferation of the colonic epithelium was studied in a 1,2-dimethylhydrazine (DMH)-induced murine carcinogenesis model. Four groups of mice, control, LCA, DMH and DMH+LCA, were studied for 4 weeks, a period corresponding to early stages of carcinogenesis. Apoptosis (AI) and proliferation (PI) indices in the colon were determined by immunohistochemistry. LCA stimulated apoptosis (AI = 1.2 ± 0.3% (all values are the mean ± SEM) versus control 0.5 ± 0.1%, P < 0.05), as did DMH (4.3 ± 0.8%, P < 0.02). DMH increased apoptosis at the base of the crypt nearly 50-fold, with no effect at the lumenal third. In mice receiving DMH, LCA suppressed apoptosis almost completely (0.1 ± 0.03%); this suppression was complete at the lower two-thirds of the crypt (AI = 0) and 60% at the lumenal third. LCA increased proliferation (PI = 22.2 ± 4.6% versus 15.4 ± 1% in controls), but this did not reach statistical significance. DMH increased proliferation (PI = 34.6 ± 2.3%, P < 0.01). In mice receiving DMH, proliferation (41 ± 2.9%) was about two-thirds of the additive effect. LCA affected proliferation, mainly in the middle third of the crypt; DMH's effect was similar in distribution, but more pronounced. In mice receiving DMH, LCA shifts proliferation upward, extending it to the lumenal third of the crypt. LCA's main cell kinetic effect in the colon is on apoptosis; this effect differs in normal (stimulation) and pre-malignant colon (nearly complete suppression). LCA does not significantly stimulate proliferation in either normal or pre-malignant colon. The differential effect of LCA on apoptosis in the presence of a carcinogen partially explains its effect as a promoter on colon carcinogenesis in animal models, and may have important implications for human carcinogenesis. Key words AI, apoptosis index DMH, 1,2-dimethylhydrazine LCA, lithocholic acid PCNA, proliferating cell nuclear antigen PI, proliferation index RT, room temperature TUNEL, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling. © Oxford University Press « Previous | Next Article » Table of Contents This Article Carcinogenesis (2000) 21 (5): 999-1005. doi: 10.1093/carcin/21.5.999 » Abstract Free Full Text (HTML) Free Full Text (PDF) Free Classifications Carcinogenesis Services Article metrics Alert me when cited Alert me if corrected Find similar articles Similar articles in Web of Science Similar articles in PubMed Add to my archive Download citation Request Permissions Citing Articles Load citing article information Citing articles via CrossRef Citing articles via Scopus Citing articles via Web of Science Citing articles via Google Scholar Google Scholar Articles by Kozoni, V. Articles by Rigas, B. Search for related content PubMed PubMed citation Articles by Kozoni, V. Articles by Tsioulias, G. Articles by Shiff, S. Articles by Rigas, B. Related Content Load related web page information Share Email this article CiteULike Delicious Facebook Google+ Mendeley Twitter What's this? Search this journal: Advanced » Current Issue October 2015 36 (10) Alert me to new issues The Journal About this journal Rights & Permissions Dispatch date of the next issue This journal is a member of the Committee on Publication Ethics (COPE) We are mobile – find out more Journals Career Network Impact factor: 5.334 5-Yr impact factor: 5.698 Editor-in-Chief Dr Curtis C Harris, USA View full editorial board For Authors Instructions to authors Online submission Submit Now! Self archiving policy Open access options for authors - visit Oxford Open This journal enables compliance with the NIH Public Access Policy Alerting Services Email table of contents Email Advance Access CiteTrack XML RSS feed Corporate Services Advertising sales Reprints Supplements var taxonomies = ("MED00710"); Most Most Read Apoptosis in cancer Modulation of E-cadherin expression by K-Ras; involvement of DNA methyltransferase-3b Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead Tumor progression and metastasis Cancer-related inflammation, the seventh hallmark of cancer: links to genetic instability » View all Most Read articles Most Cited Oxyradicals and DNA damage Sensing and repairing DNA double-strand breaks Functional role of estrogen metabolism in target cells: review and perspectives Apoptosis in cancer Nucleotide excision repair and human syndromes » View all Most Cited articles Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department. Online ISSN 1460-2180 - Print ISSN 0143-3334 Copyright © 2015 Oxford University Press Oxford Journals Oxford University Press Site Map Privacy Policy Cookie Policy Legal Notices Frequently Asked Questions Other Oxford University Press sites: Oxford University Press Oxford Journals China Oxford Journals Japan Academic & Professional books Children's & Schools Books Dictionaries & Reference Dictionary of National Biography Digital Reference English Language Teaching Higher Education Textbooks International Education Unit Law Medicine Music Online Products & Publishing Oxford Bibliographies Online Oxford Dictionaries Online Oxford English Dictionary Oxford Language Dictionaries Online Oxford Scholarship Online Reference Rights and Permissions Resources for Retailers & Wholesalers Resources for the Healthcare Industry Very Short Introductions World's Classics function fnc_onDomLoaded() { var query_context = getQueryContext(); PF_initOIUnderbar(query_context,":QS:default","","JRN"); PF_insertOIUnderbar(0); }; if (window.addEventListener) { window.addEventListener('load', fnc_onDomLoaded, false); } else if (window.attachEvent) { window.attachEvent('onload', fnc_onDomLoaded); } var gaJsHost = (("https:" == document.location.protocol) ? "https://ssl." : "http://www."); document.write(unescape("%3Cscript src='" + gaJsHost + "google-analytics.com/ga.js' type='text/javascript'%3E%3C/script%3E")); try { var pageTracker = _gat._getTracker("UA-189672-16"); pageTracker._setDomainName(".oxfordjournals.org"); pageTracker._trackPageview(); } catch(err) {}

Journal

CarcinogenesisOxford University Press

Published: May 1, 2000

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