Carbonyl Reductase 3 (CBR3) Mediates 9-cis-Retinoic Acid-Induced Cytostatis and is a Potential Prognostic Marker for Oral Malignancy

The molecular mechanisms of growth suppression by retinoic acid (RA) were examined. Our results suggest that the cytostatic effects of RA could be mediated by the activation of endogenous CBR3 gene in oral squamous cell carcinomas (OSCCs), and the expression is a potential marker for oral malignancy...

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Autores principales: Ohkura-Hada, Shuri, Kondoh, Nobuo, Hada, Akiyuki, Arai, Masaaki, Yamazaki, Yutaka, Shindoh, Masanobu, Kitagawa, Yoshimasa, Takahashi, Masayuki, Ando, Toshifumi, Sato, Yasunori, Yamamoto, Mikio
Formato: Texto
Lenguaje:English
Publicado: Bentham Open 2008
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581532/
https://www.ncbi.nlm.nih.gov/pubmed/19088887
http://dx.doi.org/10.2174/1874210600802010078
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author Ohkura-Hada, Shuri
Kondoh, Nobuo
Hada, Akiyuki
Arai, Masaaki
Yamazaki, Yutaka
Shindoh, Masanobu
Kitagawa, Yoshimasa
Takahashi, Masayuki
Ando, Toshifumi
Sato, Yasunori
Yamamoto, Mikio
author_facet Ohkura-Hada, Shuri
Kondoh, Nobuo
Hada, Akiyuki
Arai, Masaaki
Yamazaki, Yutaka
Shindoh, Masanobu
Kitagawa, Yoshimasa
Takahashi, Masayuki
Ando, Toshifumi
Sato, Yasunori
Yamamoto, Mikio
author_sort Ohkura-Hada, Shuri
collection PubMed
description The molecular mechanisms of growth suppression by retinoic acid (RA) were examined. Our results suggest that the cytostatic effects of RA could be mediated by the activation of endogenous CBR3 gene in oral squamous cell carcinomas (OSCCs), and the expression is a potential marker for oral malignancy.
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spelling pubmed-25815322008-12-16 Carbonyl Reductase 3 (CBR3) Mediates 9-cis-Retinoic Acid-Induced Cytostatis and is a Potential Prognostic Marker for Oral Malignancy Ohkura-Hada, Shuri Kondoh, Nobuo Hada, Akiyuki Arai, Masaaki Yamazaki, Yutaka Shindoh, Masanobu Kitagawa, Yoshimasa Takahashi, Masayuki Ando, Toshifumi Sato, Yasunori Yamamoto, Mikio Open Dent J Article The molecular mechanisms of growth suppression by retinoic acid (RA) were examined. Our results suggest that the cytostatic effects of RA could be mediated by the activation of endogenous CBR3 gene in oral squamous cell carcinomas (OSCCs), and the expression is a potential marker for oral malignancy. Bentham Open 2008-06-09 /pmc/articles/PMC2581532/ /pubmed/19088887 http://dx.doi.org/10.2174/1874210600802010078 Text en © Ohkura-Hada et al.; Licensee Bentham Open. http://creativecommons.org/licenses/by/2.5/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Article
Ohkura-Hada, Shuri
Kondoh, Nobuo
Hada, Akiyuki
Arai, Masaaki
Yamazaki, Yutaka
Shindoh, Masanobu
Kitagawa, Yoshimasa
Takahashi, Masayuki
Ando, Toshifumi
Sato, Yasunori
Yamamoto, Mikio
Carbonyl Reductase 3 (CBR3) Mediates 9-cis-Retinoic Acid-Induced Cytostatis and is a Potential Prognostic Marker for Oral Malignancy
title Carbonyl Reductase 3 (CBR3) Mediates 9-cis-Retinoic Acid-Induced Cytostatis and is a Potential Prognostic Marker for Oral Malignancy
title_full Carbonyl Reductase 3 (CBR3) Mediates 9-cis-Retinoic Acid-Induced Cytostatis and is a Potential Prognostic Marker for Oral Malignancy
title_fullStr Carbonyl Reductase 3 (CBR3) Mediates 9-cis-Retinoic Acid-Induced Cytostatis and is a Potential Prognostic Marker for Oral Malignancy
title_full_unstemmed Carbonyl Reductase 3 (CBR3) Mediates 9-cis-Retinoic Acid-Induced Cytostatis and is a Potential Prognostic Marker for Oral Malignancy
title_short Carbonyl Reductase 3 (CBR3) Mediates 9-cis-Retinoic Acid-Induced Cytostatis and is a Potential Prognostic Marker for Oral Malignancy
title_sort carbonyl reductase 3 (cbr3) mediates 9-cis-retinoic acid-induced cytostatis and is a potential prognostic marker for oral malignancy
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581532/
https://www.ncbi.nlm.nih.gov/pubmed/19088887
http://dx.doi.org/10.2174/1874210600802010078
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