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EBV reactivation as a target of luteolin to repress NPC tumorigenesis
Nasopharyngeal carcinoma (NPC) is a malignancy derived from the epithelial cells of the nasopharynx. Although a combination of radiotherapy with chemotherapy is effective for therapy, relapse and metastasis after remission remain major causes of mortality. Epstein-Barr virus (EBV) is believed to be...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4951347/ https://www.ncbi.nlm.nih.gov/pubmed/26967558 http://dx.doi.org/10.18632/oncotarget.7967 |
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author | Wu, Chung-Chun Fang, Chih-Yeu Hsu, Hui-Yu Chuang, Hsin-Ying Cheng, Yu-Jhen Chen, Yen-Ju Chou, Sheng-Ping Huang, Sheng-Yen Lin, Su-Fang Chang, Yao Tsai, Ching-Hwa Chen, Jen-Yang |
author_facet | Wu, Chung-Chun Fang, Chih-Yeu Hsu, Hui-Yu Chuang, Hsin-Ying Cheng, Yu-Jhen Chen, Yen-Ju Chou, Sheng-Ping Huang, Sheng-Yen Lin, Su-Fang Chang, Yao Tsai, Ching-Hwa Chen, Jen-Yang |
author_sort | Wu, Chung-Chun |
collection | PubMed |
description | Nasopharyngeal carcinoma (NPC) is a malignancy derived from the epithelial cells of the nasopharynx. Although a combination of radiotherapy with chemotherapy is effective for therapy, relapse and metastasis after remission remain major causes of mortality. Epstein-Barr virus (EBV) is believed to be one of causes of NPC development. We demonstrated previously that EBV reactivation is important for the carcinogenesis of NPC. We sought, therefore, to determine whether EBV reactivation can be a target for retardation of relapse of NPC. After screening, we found luteolin is able to inhibit EBV reactivation. It inhibited EBV lytic protein expression and repressed the promoter activities of two major immediate-early genes, Zta and Rta. Furthermore, luteolin was shown to reduce genomic instability induced by recurrent EBV reactivation in NPC cells. EBV reactivation-induced NPC cell proliferation and migration, as well as matrigel invasiveness, were also repressed by luteolin treatment. Tumorigenicity in mice, induced by EBV reactivation, was decreased profoundly following luteolin administration. Together, these results suggest that inhibition of EBV reactivation is a novel approach to prevent the relapse of NPC. |
format | Online Article Text |
id | pubmed-4951347 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-49513472016-07-21 EBV reactivation as a target of luteolin to repress NPC tumorigenesis Wu, Chung-Chun Fang, Chih-Yeu Hsu, Hui-Yu Chuang, Hsin-Ying Cheng, Yu-Jhen Chen, Yen-Ju Chou, Sheng-Ping Huang, Sheng-Yen Lin, Su-Fang Chang, Yao Tsai, Ching-Hwa Chen, Jen-Yang Oncotarget Research Paper Nasopharyngeal carcinoma (NPC) is a malignancy derived from the epithelial cells of the nasopharynx. Although a combination of radiotherapy with chemotherapy is effective for therapy, relapse and metastasis after remission remain major causes of mortality. Epstein-Barr virus (EBV) is believed to be one of causes of NPC development. We demonstrated previously that EBV reactivation is important for the carcinogenesis of NPC. We sought, therefore, to determine whether EBV reactivation can be a target for retardation of relapse of NPC. After screening, we found luteolin is able to inhibit EBV reactivation. It inhibited EBV lytic protein expression and repressed the promoter activities of two major immediate-early genes, Zta and Rta. Furthermore, luteolin was shown to reduce genomic instability induced by recurrent EBV reactivation in NPC cells. EBV reactivation-induced NPC cell proliferation and migration, as well as matrigel invasiveness, were also repressed by luteolin treatment. Tumorigenicity in mice, induced by EBV reactivation, was decreased profoundly following luteolin administration. Together, these results suggest that inhibition of EBV reactivation is a novel approach to prevent the relapse of NPC. Impact Journals LLC 2016-03-08 /pmc/articles/PMC4951347/ /pubmed/26967558 http://dx.doi.org/10.18632/oncotarget.7967 Text en Copyright: © 2016 Wu et al. http://creativecommons.org/licenses/by/2.5/ 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 credited. |
spellingShingle | Research Paper Wu, Chung-Chun Fang, Chih-Yeu Hsu, Hui-Yu Chuang, Hsin-Ying Cheng, Yu-Jhen Chen, Yen-Ju Chou, Sheng-Ping Huang, Sheng-Yen Lin, Su-Fang Chang, Yao Tsai, Ching-Hwa Chen, Jen-Yang EBV reactivation as a target of luteolin to repress NPC tumorigenesis |
title | EBV reactivation as a target of luteolin to repress NPC tumorigenesis |
title_full | EBV reactivation as a target of luteolin to repress NPC tumorigenesis |
title_fullStr | EBV reactivation as a target of luteolin to repress NPC tumorigenesis |
title_full_unstemmed | EBV reactivation as a target of luteolin to repress NPC tumorigenesis |
title_short | EBV reactivation as a target of luteolin to repress NPC tumorigenesis |
title_sort | ebv reactivation as a target of luteolin to repress npc tumorigenesis |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4951347/ https://www.ncbi.nlm.nih.gov/pubmed/26967558 http://dx.doi.org/10.18632/oncotarget.7967 |
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