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Protective effects of thioredoxin-mediated p53 activation in response to mild hyperthermia

Protective effects of thioredoxin-mediated p53 activation in response to mild hyperthermia Recently, mild hyperthermia was shown to induce cell cycle arrest at the G2/M phase transition without leading to DNA damage. The mechanism of this regulation has not yet been elucidated, although p53 has been shown to be activated in response to mild hyperthermia. Here, we report the role of thioredoxin (TXN) in mild hyperthermia-induced cellular responses. Our data showed that the protein levels of p53 and its downstream gene, Gadd45a, which is an indicator of G2/M arrest, were significantly decreased in TXN siRNA-treated cells under conditions of mild hyperthermia (41˚C, 60 min) as compared to TXN wild-type cells, implying that TXN might play an important role in mild hyperthermia-induced G2/M arrest via p53 and Gadd45a activation. Furthermore, the release of cyclin-dependent kinase Cdc2, known to be regulated by Gadd45a under G2/M arrest, was inhibited from the nucleus for arrest in the G2/M phase in TXN downregulated cells under mild hyperthermia. We suggest that G2/M arrest mediated via the TXN-modulated p53 in response to mild hyperthermia may provide critical insight into the clinical use of mild hyperthermia to induce an adaptive response against genotoxic stresses. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Oncology Reports Spandidos Publications

Protective effects of thioredoxin-mediated p53 activation in response to mild hyperthermia

Jung, Hwa Jin; Seo, Young Rok
Oncology Reports , Volume 27 (3) – Mar 1, 2012
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References (39)

Publisher
Spandidos Publications
Copyright
Copyright © Spandidos Publications
ISSN
1021-335X
eISSN
1791-2431
DOI
10.3892/or.2011.1564
pmid
22134635
Publisher site
See Article on Publisher Site

Abstract

Recently, mild hyperthermia was shown to induce cell cycle arrest at the G2/M phase transition without leading to DNA damage. The mechanism of this regulation has not yet been elucidated, although p53 has been shown to be activated in response to mild hyperthermia. Here, we report the role of thioredoxin (TXN) in mild hyperthermia-induced cellular responses. Our data showed that the protein levels of p53 and its downstream gene, Gadd45a, which is an indicator of G2/M arrest, were significantly decreased in TXN siRNA-treated cells under conditions of mild hyperthermia (41˚C, 60 min) as compared to TXN wild-type cells, implying that TXN might play an important role in mild hyperthermia-induced G2/M arrest via p53 and Gadd45a activation. Furthermore, the release of cyclin-dependent kinase Cdc2, known to be regulated by Gadd45a under G2/M arrest, was inhibited from the nucleus for arrest in the G2/M phase in TXN downregulated cells under mild hyperthermia. We suggest that G2/M arrest mediated via the TXN-modulated p53 in response to mild hyperthermia may provide critical insight into the clinical use of mild hyperthermia to induce an adaptive response against genotoxic stresses.

Journal

Oncology Reports – Spandidos Publications

Published: Mar 1, 2012

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