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Article: The emerging roles of N6-methyladenosine (m6A) deregulation in liver carcinogenesis

TitleThe emerging roles of N6-methyladenosine (m6A) deregulation in liver carcinogenesis
Authors
KeywordsHepatocellular carcinoma
N6-methyladenosine
RNA epigenetics
Epi-transcriptome
Issue Date2020
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.molecular-cancer.com
Citation
Molecular Cancer, 2020, v. 19, p. article no. 44 How to Cite?
AbstractLiver cancer is a common cancer worldwide. Although the etiological factors of liver carcinogenesis are well defined, the underlying molecular mechanisms remain largely elusive. Epigenetic deregulations, such as aberrant DNA methylation and histone modifications, play a critical role in liver carcinogenesis. Analogous to DNA and core histone proteins, reversible chemical modifications on mRNA have recently been recognized as important regulatory mechanisms to control gene expression. N6-methyladenosine (m6A) is the most prevalent internal mRNA modification in mammalian cells. m6A modification is important for controlling many cellular and biological processes. Deregulation of m6A modification has been recently implicated in human carcinogenesis, including liver cancer. In this review, we summarize the recent findings on m6A regulation and its biological impacts in normal and cancer cells. We will focus on the deregulation of m6A modification and m6A regulators in liver diseases and liver cancers. We will highlight the clinical relevance of m6A deregulation in liver cancer. We will also discuss the potential of exploiting m6A modification for cancer diagnosis and therapeutics.
DescriptionHepatocellular carcinoma
Persistent Identifierhttp://hdl.handle.net/10722/293873
ISSN
2021 Impact Factor: 41.444
2020 SCImago Journal Rankings: 7.274
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChen, M-
dc.contributor.authorWong, CM-
dc.date.accessioned2020-11-23T08:23:02Z-
dc.date.available2020-11-23T08:23:02Z-
dc.date.issued2020-
dc.identifier.citationMolecular Cancer, 2020, v. 19, p. article no. 44-
dc.identifier.issn1476-4598-
dc.identifier.urihttp://hdl.handle.net/10722/293873-
dc.descriptionHepatocellular carcinoma-
dc.description.abstractLiver cancer is a common cancer worldwide. Although the etiological factors of liver carcinogenesis are well defined, the underlying molecular mechanisms remain largely elusive. Epigenetic deregulations, such as aberrant DNA methylation and histone modifications, play a critical role in liver carcinogenesis. Analogous to DNA and core histone proteins, reversible chemical modifications on mRNA have recently been recognized as important regulatory mechanisms to control gene expression. N6-methyladenosine (m6A) is the most prevalent internal mRNA modification in mammalian cells. m6A modification is important for controlling many cellular and biological processes. Deregulation of m6A modification has been recently implicated in human carcinogenesis, including liver cancer. In this review, we summarize the recent findings on m6A regulation and its biological impacts in normal and cancer cells. We will focus on the deregulation of m6A modification and m6A regulators in liver diseases and liver cancers. We will highlight the clinical relevance of m6A deregulation in liver cancer. We will also discuss the potential of exploiting m6A modification for cancer diagnosis and therapeutics.-
dc.languageeng-
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.molecular-cancer.com-
dc.relation.ispartofMolecular Cancer-
dc.rightsMolecular Cancer. Copyright © BioMed Central Ltd.-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectHepatocellular carcinoma-
dc.subjectN6-methyladenosine-
dc.subjectRNA epigenetics-
dc.subjectEpi-transcriptome-
dc.titleThe emerging roles of N6-methyladenosine (m6A) deregulation in liver carcinogenesis-
dc.typeArticle-
dc.identifier.emailWong, CM: jcmwong@hku.hk-
dc.identifier.authorityWong, CM=rp00231-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/s12943-020-01172-y-
dc.identifier.pmid32111216-
dc.identifier.pmcidPMC7047367-
dc.identifier.scopuseid_2-s2.0-85080969170-
dc.identifier.hkuros320057-
dc.identifier.volume19-
dc.identifier.spagearticle no. 44-
dc.identifier.epagearticle no. 44-
dc.identifier.isiWOS:000518909200002-
dc.publisher.placeUnited Kingdom-

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