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Regulation of Cell Transformation by Rb-Controlled Redox Homeostasis

Rb is a tumor suppressor, and regulates various biological progresses, such as cell proliferation, development, metabolism and cell death. In the current study, we show that Rb knockout in 3T3 cells leads to oxidative redox state and low mitochondrial membrane potential by regulating mitochondrial a...

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Detalles Bibliográficos
Autores principales: Zhu, Zhongling, Wang, Yuanyuan, Liang, Zheng, Wang, Wenwen, Zhang, Huamei, Li, Binghui, Ying, Guoguang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4097070/
https://www.ncbi.nlm.nih.gov/pubmed/25019272
http://dx.doi.org/10.1371/journal.pone.0102582
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author Zhu, Zhongling
Wang, Yuanyuan
Liang, Zheng
Wang, Wenwen
Zhang, Huamei
Li, Binghui
Ying, Guoguang
author_facet Zhu, Zhongling
Wang, Yuanyuan
Liang, Zheng
Wang, Wenwen
Zhang, Huamei
Li, Binghui
Ying, Guoguang
author_sort Zhu, Zhongling
collection PubMed
description Rb is a tumor suppressor, and regulates various biological progresses, such as cell proliferation, development, metabolism and cell death. In the current study, we show that Rb knockout in 3T3 cells leads to oxidative redox state and low mitochondrial membrane potential by regulating mitochondrial activity. Our results indicate that Rb plays an important role in controlling redox homeostasis. More importantly, the functions of Rb in modulating cell proliferation, death and transformation are, at least in part, mediated by its controlling cellular redox state. In addition, our results also suggest that the cellular redox state possibly determines various biological activities, including cell survival, death and transformation, where Rb is functioning as a regulator of redox homeostasis.
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spelling pubmed-40970702014-07-17 Regulation of Cell Transformation by Rb-Controlled Redox Homeostasis Zhu, Zhongling Wang, Yuanyuan Liang, Zheng Wang, Wenwen Zhang, Huamei Li, Binghui Ying, Guoguang PLoS One Research Article Rb is a tumor suppressor, and regulates various biological progresses, such as cell proliferation, development, metabolism and cell death. In the current study, we show that Rb knockout in 3T3 cells leads to oxidative redox state and low mitochondrial membrane potential by regulating mitochondrial activity. Our results indicate that Rb plays an important role in controlling redox homeostasis. More importantly, the functions of Rb in modulating cell proliferation, death and transformation are, at least in part, mediated by its controlling cellular redox state. In addition, our results also suggest that the cellular redox state possibly determines various biological activities, including cell survival, death and transformation, where Rb is functioning as a regulator of redox homeostasis. Public Library of Science 2014-07-14 /pmc/articles/PMC4097070/ /pubmed/25019272 http://dx.doi.org/10.1371/journal.pone.0102582 Text en © 2014 Zhu et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Zhu, Zhongling
Wang, Yuanyuan
Liang, Zheng
Wang, Wenwen
Zhang, Huamei
Li, Binghui
Ying, Guoguang
Regulation of Cell Transformation by Rb-Controlled Redox Homeostasis
title Regulation of Cell Transformation by Rb-Controlled Redox Homeostasis
title_full Regulation of Cell Transformation by Rb-Controlled Redox Homeostasis
title_fullStr Regulation of Cell Transformation by Rb-Controlled Redox Homeostasis
title_full_unstemmed Regulation of Cell Transformation by Rb-Controlled Redox Homeostasis
title_short Regulation of Cell Transformation by Rb-Controlled Redox Homeostasis
title_sort regulation of cell transformation by rb-controlled redox homeostasis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4097070/
https://www.ncbi.nlm.nih.gov/pubmed/25019272
http://dx.doi.org/10.1371/journal.pone.0102582
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