The ING4 Binding with p53 and Induced p53 Acetylation were Attenuated by Human Papillomavirus 16 E6

High risk subtype HPV16 early oncoprotein E6 contributes host cell immortalization and transformation through interacting with a number of cellular factors. ING4 is one member of the inhibitor of growth (ING) family of type II tumor suppressors and it has been shown to be involved in regulating p53...

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Autores principales: Guo, Yi, Meng, Xiangkai, Wang, Qian, Wang, Yanan, Shang, Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742747/
https://www.ncbi.nlm.nih.gov/pubmed/23967213
http://dx.doi.org/10.1371/journal.pone.0071453
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author Guo, Yi
Meng, Xiangkai
Wang, Qian
Wang, Yanan
Shang, Hong
author_facet Guo, Yi
Meng, Xiangkai
Wang, Qian
Wang, Yanan
Shang, Hong
author_sort Guo, Yi
collection PubMed
description High risk subtype HPV16 early oncoprotein E6 contributes host cell immortalization and transformation through interacting with a number of cellular factors. ING4 is one member of the inhibitor of growth (ING) family of type II tumor suppressors and it has been shown to be involved in regulating p53 function. However, the effect and mechanism of HPV16 E6 on ING4 function remain elusive. In this study, we report HPV16 E6 combines with ING4 in vivo and in vitro. The ING4 induced p53 acetylation and its combining with p53 were attenuated by HPV16 E6 independent of p53 degradation. The enhancing function of ING4 on p53 mediated apoptosis was diminished when HPV16 E6 existed. These findings reveal that ING4 may be a common target of oncogenic viruses for driving host cell carcinogenesis.
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spelling pubmed-37427472013-08-21 The ING4 Binding with p53 and Induced p53 Acetylation were Attenuated by Human Papillomavirus 16 E6 Guo, Yi Meng, Xiangkai Wang, Qian Wang, Yanan Shang, Hong PLoS One Research Article High risk subtype HPV16 early oncoprotein E6 contributes host cell immortalization and transformation through interacting with a number of cellular factors. ING4 is one member of the inhibitor of growth (ING) family of type II tumor suppressors and it has been shown to be involved in regulating p53 function. However, the effect and mechanism of HPV16 E6 on ING4 function remain elusive. In this study, we report HPV16 E6 combines with ING4 in vivo and in vitro. The ING4 induced p53 acetylation and its combining with p53 were attenuated by HPV16 E6 independent of p53 degradation. The enhancing function of ING4 on p53 mediated apoptosis was diminished when HPV16 E6 existed. These findings reveal that ING4 may be a common target of oncogenic viruses for driving host cell carcinogenesis. Public Library of Science 2013-08-13 /pmc/articles/PMC3742747/ /pubmed/23967213 http://dx.doi.org/10.1371/journal.pone.0071453 Text en © 2013 Guo 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
Guo, Yi
Meng, Xiangkai
Wang, Qian
Wang, Yanan
Shang, Hong
The ING4 Binding with p53 and Induced p53 Acetylation were Attenuated by Human Papillomavirus 16 E6
title The ING4 Binding with p53 and Induced p53 Acetylation were Attenuated by Human Papillomavirus 16 E6
title_full The ING4 Binding with p53 and Induced p53 Acetylation were Attenuated by Human Papillomavirus 16 E6
title_fullStr The ING4 Binding with p53 and Induced p53 Acetylation were Attenuated by Human Papillomavirus 16 E6
title_full_unstemmed The ING4 Binding with p53 and Induced p53 Acetylation were Attenuated by Human Papillomavirus 16 E6
title_short The ING4 Binding with p53 and Induced p53 Acetylation were Attenuated by Human Papillomavirus 16 E6
title_sort ing4 binding with p53 and induced p53 acetylation were attenuated by human papillomavirus 16 e6
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742747/
https://www.ncbi.nlm.nih.gov/pubmed/23967213
http://dx.doi.org/10.1371/journal.pone.0071453
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