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Smad3 mutant mice develop colon cancer with overexpression of COX-2

Colon cancer is the second most common cause of cancer-associated mortality in human populations. The aim of the present study was to identify the role of cyclooxygenase-2 (COX-2) in Smad3 mutant mice, which are known to develop colon cancer. Homozygous Smad3 (−/−) mutant mice were generated from in...

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Autores principales: Zhu, Yu-Ping, Liu, Zhuo, Fu, Zhi-Xuan, Li, De-Chuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5403702/
https://www.ncbi.nlm.nih.gov/pubmed/28454287
http://dx.doi.org/10.3892/ol.2017.5639
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author Zhu, Yu-Ping
Liu, Zhuo
Fu, Zhi-Xuan
Li, De-Chuan
author_facet Zhu, Yu-Ping
Liu, Zhuo
Fu, Zhi-Xuan
Li, De-Chuan
author_sort Zhu, Yu-Ping
collection PubMed
description Colon cancer is the second most common cause of cancer-associated mortality in human populations. The aim of the present study was to identify the role of cyclooxygenase-2 (COX-2) in Smad3 mutant mice, which are known to develop colon cancer. Homozygous Smad3 (−/−) mutant mice were generated from inbred and hybrid Smad3 mouse strains by intercrossing the appropriate heterozygotes. Immunohistochemistry with COX-2 antibody was performed throughout this experiment and the data was validated and cross-checked with reverse transcription-polymerase chain reaction (RT-PCR). Homozygous mutant Smad3 mice were generated and the overexpression pattern of COX-2 was identified by immunohistochemistry and validated with RT-PCR. The results of the present study demonstrated a link between the Smad3 mutant mice, colon cancer and COX-2. In addition, the overexpression pattern of COX-2 in Smad3 mutant mice that develop colon cancer was identified.
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spelling pubmed-54037022017-04-27 Smad3 mutant mice develop colon cancer with overexpression of COX-2 Zhu, Yu-Ping Liu, Zhuo Fu, Zhi-Xuan Li, De-Chuan Oncol Lett Articles Colon cancer is the second most common cause of cancer-associated mortality in human populations. The aim of the present study was to identify the role of cyclooxygenase-2 (COX-2) in Smad3 mutant mice, which are known to develop colon cancer. Homozygous Smad3 (−/−) mutant mice were generated from inbred and hybrid Smad3 mouse strains by intercrossing the appropriate heterozygotes. Immunohistochemistry with COX-2 antibody was performed throughout this experiment and the data was validated and cross-checked with reverse transcription-polymerase chain reaction (RT-PCR). Homozygous mutant Smad3 mice were generated and the overexpression pattern of COX-2 was identified by immunohistochemistry and validated with RT-PCR. The results of the present study demonstrated a link between the Smad3 mutant mice, colon cancer and COX-2. In addition, the overexpression pattern of COX-2 in Smad3 mutant mice that develop colon cancer was identified. D.A. Spandidos 2017-03 2017-01-25 /pmc/articles/PMC5403702/ /pubmed/28454287 http://dx.doi.org/10.3892/ol.2017.5639 Text en Copyright: © Zhu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Zhu, Yu-Ping
Liu, Zhuo
Fu, Zhi-Xuan
Li, De-Chuan
Smad3 mutant mice develop colon cancer with overexpression of COX-2
title Smad3 mutant mice develop colon cancer with overexpression of COX-2
title_full Smad3 mutant mice develop colon cancer with overexpression of COX-2
title_fullStr Smad3 mutant mice develop colon cancer with overexpression of COX-2
title_full_unstemmed Smad3 mutant mice develop colon cancer with overexpression of COX-2
title_short Smad3 mutant mice develop colon cancer with overexpression of COX-2
title_sort smad3 mutant mice develop colon cancer with overexpression of cox-2
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5403702/
https://www.ncbi.nlm.nih.gov/pubmed/28454287
http://dx.doi.org/10.3892/ol.2017.5639
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