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Article: The functional role of long noncoding RNA in resistance to anticancer treatment

TitleThe functional role of long noncoding RNA in resistance to anticancer treatment
Authors
Keywordscancer
drug resistance
EMT
long noncoding RNAs
mechanisms
Issue Date2020
PublisherSAGE Publications (UK and US): Open Access Titles. The Journal's web site is located at https://journals.sagepub.com/home/tama
Citation
Therapeutic Advances in Medical Oncology, 2020, v. 12, p. article no. 1758835920927850 How to Cite?
AbstractChemotherapy is one of the fundamental methods of cancer treatment. However, drug resistance remains the main cause of clinical treatment failure. We comprehensively review the newly identified roles of long noncoding RNAs (lncRNAs) in oncobiology that are associated with drug resistance. The expression of lncRNAs is tissue-specific and often dysregulated in human cancers. Accumulating evidence suggests that lncRNAs are involved in chemoresistance of cancer cells. The main lncRNA-driven mechanisms of chemoresistance include regulation of drug efflux, DNA damage repair, cell cycle, apoptosis, epithelial-mesenchymal transition (EMT), induction of signaling pathways, and angiogenesis. LncRNA-driven mechanisms of resistance to various antineoplastic agents have been studied extensively. There are unique mechanisms of resistance against different types of drugs, and each mechanism may have more than one contributing factor. We summarize the emerging strategies that can be used to overcome the technical challenges in studying and addressing lncRNA-mediated drug resistance.
Persistent Identifierhttp://hdl.handle.net/10722/284280
ISSN
2020 Impact Factor: 8.168
2015 SCImago Journal Rankings: 1.407
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorQU, Y-
dc.contributor.authorTan, HY-
dc.contributor.authorChan, YT-
dc.contributor.authorJIANG, H-
dc.contributor.authorWang, N-
dc.contributor.authorWANG, D-
dc.date.accessioned2020-07-20T05:57:28Z-
dc.date.available2020-07-20T05:57:28Z-
dc.date.issued2020-
dc.identifier.citationTherapeutic Advances in Medical Oncology, 2020, v. 12, p. article no. 1758835920927850-
dc.identifier.issn1758-8340-
dc.identifier.urihttp://hdl.handle.net/10722/284280-
dc.description.abstractChemotherapy is one of the fundamental methods of cancer treatment. However, drug resistance remains the main cause of clinical treatment failure. We comprehensively review the newly identified roles of long noncoding RNAs (lncRNAs) in oncobiology that are associated with drug resistance. The expression of lncRNAs is tissue-specific and often dysregulated in human cancers. Accumulating evidence suggests that lncRNAs are involved in chemoresistance of cancer cells. The main lncRNA-driven mechanisms of chemoresistance include regulation of drug efflux, DNA damage repair, cell cycle, apoptosis, epithelial-mesenchymal transition (EMT), induction of signaling pathways, and angiogenesis. LncRNA-driven mechanisms of resistance to various antineoplastic agents have been studied extensively. There are unique mechanisms of resistance against different types of drugs, and each mechanism may have more than one contributing factor. We summarize the emerging strategies that can be used to overcome the technical challenges in studying and addressing lncRNA-mediated drug resistance.-
dc.languageeng-
dc.publisherSAGE Publications (UK and US): Open Access Titles. The Journal's web site is located at https://journals.sagepub.com/home/tama-
dc.relation.ispartofTherapeutic Advances in Medical Oncology-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectcancer-
dc.subjectdrug resistance-
dc.subjectEMT-
dc.subjectlong noncoding RNAs-
dc.subjectmechanisms-
dc.titleThe functional role of long noncoding RNA in resistance to anticancer treatment-
dc.typeArticle-
dc.identifier.emailTan, HY: hyhtan@hku.hk-
dc.identifier.emailChan, YT: ecyt1@hku.hk-
dc.identifier.emailWang, N: ckwang@hku.hk-
dc.identifier.authorityWang, N=rp02075-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1177/1758835920927850-
dc.identifier.scopuseid_2-s2.0-85085888147-
dc.identifier.hkuros311483-
dc.identifier.volume12-
dc.identifier.spagearticle no. 1758835920927850-
dc.identifier.epagearticle no. 1758835920927850-
dc.identifier.isiWOS:000539246500001-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl1758-8340-

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