Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/107708
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dc.contributor.authorLeão, Ricardo-
dc.contributor.authorApolónio, Joana Dias-
dc.contributor.authorLee, Donghyun-
dc.contributor.authorFigueiredo, Arnaldo-
dc.contributor.authorTabori, Uri-
dc.contributor.authorCastelo Branco, Pedro-
dc.date.accessioned2023-07-28T08:45:02Z-
dc.date.available2023-07-28T08:45:02Z-
dc.date.issued2018-03-12-
dc.identifier.issn1423-0127pt
dc.identifier.urihttps://hdl.handle.net/10316/107708-
dc.description.abstractBackground: Limitless self-renewal is one of the hallmarks of cancer and is attained by telomere maintenance, essentially through telomerase (hTERT) activation. Transcriptional regulation of hTERT is believed to play a major role in telomerase activation in human cancers. Main body: The dominant interest in telomerase results from its role in cancer. The role of telomeres and telomere maintenance mechanisms is well established as a major driving force in generating chromosomal and genomic instability. Cancer cells have acquired the ability to overcome their fate of senescence via telomere length maintenance mechanisms, mainly by telomerase activation. hTERT expression is up-regulated in tumors via multiple genetic and epigenetic mechanisms including hTERT amplifications, hTERT structural variants, hTERT promoter mutations and epigenetic modifications through hTERT promoter methylation. Genetic (hTERT promoter mutations) and epigenetic (hTERT promoter methylation and miRNAs) events were shown to have clinical implications in cancers that depend on hTERT activation. Knowing that telomeres are crucial for cellular self-renewal, the mechanisms responsible for telomere maintenance have a crucial role in cancer diseases and might be important oncological biomarkers. Thus, rather than quantifying TERT expression and its correlation with telomerase activation, the discovery and the assessment of the mechanisms responsible for TERT upregulation offers important information that may be used for diagnosis, prognosis, and treatment monitoring in oncology. Furthermore, a better understanding of these mechanisms may promote their translation into effective targeted cancer therapies. Conclusion: Herein, we reviewed the underlying mechanisms of hTERT regulation, their role in oncogenesis, and the potential clinical applications in telomerase-dependent cancers.pt
dc.language.isoengpt
dc.publisherSpringer Naturept
dc.relationUID/BIM/04773/2013pt
dc.relationFCT - Doctoral Grant SFRH/BD/102232/2014pt
dc.relationPD/BD/105899/2014 FCT fellowshippt
dc.rightsopenAccesspt
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt
dc.subjectTelomerespt
dc.subjectTelomerasept
dc.subjectTelomerase regulationpt
dc.subjectCancer biomarkerspt
dc.subject.meshCarcinogenesispt
dc.subject.meshGene Expression Regulation, Enzymologicpt
dc.subject.meshGene Expression Regulation, Neoplasticpt
dc.subject.meshHumanspt
dc.subject.meshNeoplasmspt
dc.subject.meshTelomerasept
dc.titleMechanisms of human telomerase reverse transcriptase (hTERT) regulation: clinical impacts in cancerpt
dc.typearticle-
degois.publication.firstPage0422pt
degois.publication.issue1pt
degois.publication.titleJournal of Biomedical Sciencept
dc.peerreviewedyespt
dc.identifier.doi10.1186/s12929-018-0422-8pt
degois.publication.volume25pt
dc.date.embargo2018-03-12*
uc.date.periodoEmbargo0pt
item.grantfulltextopen-
item.cerifentitytypePublications-
item.languageiso639-1en-
item.openairetypearticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextCom Texto completo-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.orcid0000-0003-3719-717X-
crisitem.author.orcid0000-0002-7157-0081-
crisitem.author.orcid0000-0002-5019-2683-
crisitem.author.orcid0000-0002-3453-3978-
Appears in Collections:FMUC Medicina - Artigos em Revistas Internacionais
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