Identification of HPV16-p16INK4a mediated methylation in oral potentially malignant disorder

Vista sencilla de ítem
dc.contributor.authorBuenahora, María Rosa
dc.contributor.authorLafaurie, Gloria Ines
dc.contributor.authorPerdomo Lara, Sandra Janneth
dc.contributor.orcidLafaurie, Gloria Ines [0000-0003-3986-0625]
dc.contributor.orcidPerdomo Lara, Sandra Janneth [0000-0002-4429-3760]
dc.date.accessioned2020-12-01T20:33:00Z
dc.date.available2020-12-01T20:33:00Z
dc.date.issued2020
dc.description.abstractenglishTo evaluate the possible involvement of epigenetic modulation by HPV16-p16INK4a in oral poten-tially malignant disorder (OPMD). We generated DNA-methylation profiles, according to p16INK4a expression and HPV16 genotype (positive or negative), of OPMD samples and p16INK4a-HPV16 negative samples (used as control), using reduced-representation bisulphite sequencing (RRBS- Seq- Illumina) technology. Twelve samples, four for each group, as follows: 1) p16INK4a+ HPV16 +; 2) p16INK4a+ HPV16-; 3) p16INK4a- HPV16-, were analysed in triplicate for DNA-methylation profiles. Fifty-four per cent of DMRs were hypermethylated and 46% were hypomethylated. An increase in methylation of loci in OPMD was independent of the presence of HPV. The hyper-methylated genes in HPV+ samples were associated with signalling pathways such as NICD traffics to nucleus, signalling by NOTCH1 (p = 0.008), Interferon-gamma (p = 0.008) and Interleukin-6 signalling (p = 0.027). The hypomethylated genes in HPV infection were associated with TRAF3- dependent IRF activation pathway (p = 0.002), RIG-I/MDA5 mediated induction of IFN-alpha/beta pathways (p = 0.005), TRAF6 mediated IRF7 activation (p = 0.009), TRIF-mediated TLR3/TLR4 signalling (p = 0.011) and MyD88-independent cascade release of apoptotic factors (p = 0.011). Protein association analysis of DMRs in OPMD revealed 19 genes involved in the cell cycle regulation, immune system, and focal adhesion. Aberrantly methylated loci in OPMD were observed in p16INK4a positive samples which suggests that a shift in global methylation status may be important for cancer progression. The results suggest that HPV infection in OPMD induces modulation of genes related to the immune system and regulation of the cellular cycleeng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.1080/15592294.2020.1834923
dc.identifier.instnameinstname:Universidad El Bosquespa
dc.identifier.issn1559-2308
dc.identifier.reponamereponame:Repositorio Institucional Universidad El Bosquespa
dc.identifier.repourlrepourl:https://repositorio.unbosque.edu.co
dc.identifier.urihttps://hdl.handle.net/20.500.12495/5156
dc.language.isoeng
dc.publisherTaylor & Francisspa
dc.publisher.journalEpigeneticsspa
dc.relation.ispartofseriesEpigenetics, 1559-2308, 2020spa
dc.relation.urihttps://www.tandfonline.com/doi/abs/10.1080/15592294.2020.1834923?journalCode=kepi20
dc.rights.accessrightshttps://purl.org/coar/access_right/c_abf2
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess
dc.rights.accessrightsAcceso abierto
dc.rights.creativecommons2020-11-09
dc.rights.localAcceso abiertospa
dc.subject.keywordsOral potentially malignant disorderspa
dc.subject.keywordsHuman papilloma virusspa
dc.subject.keywordsRRBSspa
dc.subject.keywordsDNAspa
dc.subject.keywordsMethylationspa
dc.subject.keywordsImmune systemspa
dc.titleIdentification of HPV16-p16INK4a mediated methylation in oral potentially malignant disorderspa
dc.title.translatedIdentification of HPV16-p16INK4a mediated methylation in oral potentially malignant disorderspa
dc.type.coarhttps://purl.org/coar/resource_type/c_6501
dc.type.driverinfo:eu-repo/semantics/article
dc.type.hasversioninfo:eu-repo/semantics/publishedVersion
dc.type.localArtículo de revista

Archivos

Bloque original
Mostrando 1 - 1 de 1
No hay miniatura disponible
Nombre:
Maria Rosa Buenahoraa, Gloria Inés Lafauri_2020.pdf
Tamaño:
7.98 MB
Formato:
Adobe Portable Document Format
Descripción:
Descargar
Bloque de licencias
Mostrando 1 - 1 de 1
No hay miniatura disponible
Nombre:
license.txt
Tamaño:
1.71 KB
Formato:
Item-specific license agreed upon to submission
Descripción:
Descargar

Colecciones

Artículos