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Epigenetic disruption of cell signaling in nasopharyngeal carcinoma

Nasopharyngeal carcinoma (NPC) is a malignancy with remarkable ethnic and geographic distribution in southern China and Southeast Asia. Alternative to genetic changes, aberrant epigenetic events disrupt multiple genes involved in cell signaling pathways through DNA methylation of promoter CpG island...

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Detalles Bibliográficos
Autores principales: Li, Li-Li, Shu, Xing-Sheng, Wang, Zhao-Hui, Cao, Ya, Tao, Qian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Sun Yat-sen University Cancer Center 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4013349/
https://www.ncbi.nlm.nih.gov/pubmed/21439244
http://dx.doi.org/10.5732/cjc.011.10080
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author Li, Li-Li
Shu, Xing-Sheng
Wang, Zhao-Hui
Cao, Ya
Tao, Qian
author_facet Li, Li-Li
Shu, Xing-Sheng
Wang, Zhao-Hui
Cao, Ya
Tao, Qian
author_sort Li, Li-Li
collection PubMed
description Nasopharyngeal carcinoma (NPC) is a malignancy with remarkable ethnic and geographic distribution in southern China and Southeast Asia. Alternative to genetic changes, aberrant epigenetic events disrupt multiple genes involved in cell signaling pathways through DNA methylation of promoter CpG islands and/or histone modifications. These epigenetic alterations grant cell growth advantage and contribute to the initiation and progression of NPC. In this review, we summarize the epigenetic deregulation of cell signaling in NPC tumorigenesis and highlight the importance of identifying epigenetic cell signaling regulators in NPC research. Developing pharmacologic strategies to reverse the epigenetic-silencing of cell signaling regulators might thus be useful to NPC prevention and therapy.
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spelling pubmed-40133492014-05-15 Epigenetic disruption of cell signaling in nasopharyngeal carcinoma Li, Li-Li Shu, Xing-Sheng Wang, Zhao-Hui Cao, Ya Tao, Qian Chin J Cancer Review Nasopharyngeal carcinoma (NPC) is a malignancy with remarkable ethnic and geographic distribution in southern China and Southeast Asia. Alternative to genetic changes, aberrant epigenetic events disrupt multiple genes involved in cell signaling pathways through DNA methylation of promoter CpG islands and/or histone modifications. These epigenetic alterations grant cell growth advantage and contribute to the initiation and progression of NPC. In this review, we summarize the epigenetic deregulation of cell signaling in NPC tumorigenesis and highlight the importance of identifying epigenetic cell signaling regulators in NPC research. Developing pharmacologic strategies to reverse the epigenetic-silencing of cell signaling regulators might thus be useful to NPC prevention and therapy. Sun Yat-sen University Cancer Center 2011-04 /pmc/articles/PMC4013349/ /pubmed/21439244 http://dx.doi.org/10.5732/cjc.011.10080 Text en Chinese Journal of Cancer http://creativecommons.org/licenses/by-nc-sa/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License, which allows readers to alter, transform, or build upon the article and then distribute the resulting work under the same or similar license to this one. The work must be attributed back to the original author and commercial use is not permitted without specific permission.
spellingShingle Review
Li, Li-Li
Shu, Xing-Sheng
Wang, Zhao-Hui
Cao, Ya
Tao, Qian
Epigenetic disruption of cell signaling in nasopharyngeal carcinoma
title Epigenetic disruption of cell signaling in nasopharyngeal carcinoma
title_full Epigenetic disruption of cell signaling in nasopharyngeal carcinoma
title_fullStr Epigenetic disruption of cell signaling in nasopharyngeal carcinoma
title_full_unstemmed Epigenetic disruption of cell signaling in nasopharyngeal carcinoma
title_short Epigenetic disruption of cell signaling in nasopharyngeal carcinoma
title_sort epigenetic disruption of cell signaling in nasopharyngeal carcinoma
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4013349/
https://www.ncbi.nlm.nih.gov/pubmed/21439244
http://dx.doi.org/10.5732/cjc.011.10080
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