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Article: Epstein-Barr Virus BART Long Non-coding RNAs Function as Epigenetic Modulators in Nasopharyngeal Carcinoma

TitleEpstein-Barr Virus BART Long Non-coding RNAs Function as Epigenetic Modulators in Nasopharyngeal Carcinoma
Authors
KeywordsEpstein-Barr virus
nasopharyngeal carcinoma
lncRNA
BART
epigenetics
Issue Date2019
PublisherFrontiers Research Foundation. The Journal's web site is located at http://www.frontiersin.org/oncology
Citation
Frontiers in Oncology, 2019, v. 9, p. article no. 1120 How to Cite?
AbstractEpstein-Barr virus (EBV) establishes lifelong latent infection in humans and is associated with several lymphoid and epithelial cancers. In nasopharyngeal carcinoma (NPC), EBV expresses few viral proteins but elevated levels of Bam-HI A rightward transcripts (BARTs) RNA, which includes viral microRNAs and long non-coding RNAs (lncRNAs). BART lncRNAs localize within the nucleus of EBV-infected cells and knockdown of BART lncRNAs significantly affects the expression of genes associated with cell adhesion, oxidoreductase activity, inflammation, and immunity. Notably, downregulation of IKAROS family zinc finger 3 (IKZF3/Aiolos), which plays a role in lymphocyte development and cell attachment, occurred in NPC C666-1 cells following BART lncRNA-knockdown. Since Aiolos expression is normally restricted to lymphoid cells and rarely observed in epithelial cells, induction of Aiolos by BART lncRNA was confirmed by expressing the major BART lncRNA isoform, RPMS1, in EBV-positive and -negative cells. BART lncRNA associated with the CBP/p300 complex and RNA polymerase II (Pol II) in the nucleus, suggesting that BART lncRNAs may mediate epigenetic regulation of gene expression through interaction with the chromatin remodeling machinery. This contention is further supported by evidence that BART lncRNA appears to stall Pol II at the promoter region and may regulate IFNB1 and CXCL8 expression by inhibiting transcription by Pol II in NPC. We hypothesize that EBV BART lncRNA expression modulates host gene expression and maintains EBV latency by interfering with histone methylation and acetylation processes. Aberrant expression of affected host genes mediated by BART lncRNA may lead to immune evasion, progression, and metastasis of NPC.
Persistent Identifierhttp://hdl.handle.net/10722/288393
ISSN
2019 Impact Factor: 4.848
2015 SCImago Journal Rankings: 2.133
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorVerhoeven, RJA-
dc.contributor.authorTong, S-
dc.contributor.authorMok, BWY-
dc.contributor.authorLIU, J-
dc.contributor.authorHe, S-
dc.contributor.authorZong, J-
dc.contributor.authorChen, Y-
dc.contributor.authorTsao, SW-
dc.contributor.authorLung, ML-
dc.contributor.authorChen, H-
dc.date.accessioned2020-10-05T12:12:13Z-
dc.date.available2020-10-05T12:12:13Z-
dc.date.issued2019-
dc.identifier.citationFrontiers in Oncology, 2019, v. 9, p. article no. 1120-
dc.identifier.issn2234-943X-
dc.identifier.urihttp://hdl.handle.net/10722/288393-
dc.description.abstractEpstein-Barr virus (EBV) establishes lifelong latent infection in humans and is associated with several lymphoid and epithelial cancers. In nasopharyngeal carcinoma (NPC), EBV expresses few viral proteins but elevated levels of Bam-HI A rightward transcripts (BARTs) RNA, which includes viral microRNAs and long non-coding RNAs (lncRNAs). BART lncRNAs localize within the nucleus of EBV-infected cells and knockdown of BART lncRNAs significantly affects the expression of genes associated with cell adhesion, oxidoreductase activity, inflammation, and immunity. Notably, downregulation of IKAROS family zinc finger 3 (IKZF3/Aiolos), which plays a role in lymphocyte development and cell attachment, occurred in NPC C666-1 cells following BART lncRNA-knockdown. Since Aiolos expression is normally restricted to lymphoid cells and rarely observed in epithelial cells, induction of Aiolos by BART lncRNA was confirmed by expressing the major BART lncRNA isoform, RPMS1, in EBV-positive and -negative cells. BART lncRNA associated with the CBP/p300 complex and RNA polymerase II (Pol II) in the nucleus, suggesting that BART lncRNAs may mediate epigenetic regulation of gene expression through interaction with the chromatin remodeling machinery. This contention is further supported by evidence that BART lncRNA appears to stall Pol II at the promoter region and may regulate IFNB1 and CXCL8 expression by inhibiting transcription by Pol II in NPC. We hypothesize that EBV BART lncRNA expression modulates host gene expression and maintains EBV latency by interfering with histone methylation and acetylation processes. Aberrant expression of affected host genes mediated by BART lncRNA may lead to immune evasion, progression, and metastasis of NPC.-
dc.languageeng-
dc.publisherFrontiers Research Foundation. The Journal's web site is located at http://www.frontiersin.org/oncology-
dc.relation.ispartofFrontiers in Oncology-
dc.rightsThis Document is Protected by copyright and was first published by Frontiers. All rights reserved. It is reproduced with permission.-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectEpstein-Barr virus-
dc.subjectnasopharyngeal carcinoma-
dc.subjectlncRNA-
dc.subjectBART-
dc.subjectepigenetics-
dc.titleEpstein-Barr Virus BART Long Non-coding RNAs Function as Epigenetic Modulators in Nasopharyngeal Carcinoma-
dc.typeArticle-
dc.identifier.emailMok, BWY: bobomok@hku.hk-
dc.identifier.emailTsao, SW: gswtsao@hku.hk-
dc.identifier.emailLung, ML: mlilung@hku.hk-
dc.identifier.emailChen, H: hlchen@hku.hk-
dc.identifier.authorityTsao, SW=rp00399-
dc.identifier.authorityLung, ML=rp00300-
dc.identifier.authorityChen, H=rp00383-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3389/fonc.2019.01120-
dc.identifier.pmid31696060-
dc.identifier.pmcidPMC6817499-
dc.identifier.scopuseid_2-s2.0-85074471271-
dc.identifier.hkuros314765-
dc.identifier.volume9-
dc.identifier.spagearticle no. 1120-
dc.identifier.epagearticle no. 1120-
dc.publisher.placeSwitzerland-

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