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Article: MiR-92 suppresses proliferation and induces apoptosis by targeting EP4/Notch 1 axis in gastric cancer

TitleMiR-92 suppresses proliferation and induces apoptosis by targeting EP4/Notch 1 axis in gastric cancer
Authors
KeywordsEP4
NF-κB
Notch1
Gastric cancer
miR-92
Issue Date2018
PublisherImpact Journals LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html
Citation
Oncotarget, 2018, v. 9 n. 36, p. 24209-24220 How to Cite?
AbstractMiR-92a has been shown to be dysregulated in various cancers and exhibited differential role in carcinogenesis. In this study, we sought to delineate the functional role of miR-92a and its regulatory pathway in gastric cancer. MiR-92a expression were underexpressed in tissues of gastric cancer patients with the area under curve (AUC) of 0.78. Low expression in plasma was due to the increased promoter DNA methylation of miR-92a. Overexpression of miR-92a inhibited cell proliferation and invasion, and induced apoptosis. Furthermore, miR-92a reduced tumor growth in xenograft model. EP4 and Notch 1 were identified to be negatively regulated by miR-92a, and involved in cell growth. Moreover, NF-κB expression was inversely correlated with miR-92a in gastric cancer tissues and suppressed the expression of miR-92. This study unravels the tumor suppressive role of miR-92a involving EP4/Notch 1 signaling regulated by NF-κB in gastric cancer. Further studies on miR-92a and EP4/Notch1 may provide a new treatment strategy for gastric cancer.
Persistent Identifierhttp://hdl.handle.net/10722/258738
ISSN
2015 Impact Factor: 5.008
2015 SCImago Journal Rankings: 2.294
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorShin, VY-
dc.contributor.authorSiu, JMT-
dc.contributor.authorLiu, X-
dc.contributor.authorNg, EKO-
dc.contributor.authorKwong, A-
dc.contributor.authorChu, KM-
dc.date.accessioned2018-08-22T01:43:15Z-
dc.date.available2018-08-22T01:43:15Z-
dc.date.issued2018-
dc.identifier.citationOncotarget, 2018, v. 9 n. 36, p. 24209-24220-
dc.identifier.issn1949-2553-
dc.identifier.urihttp://hdl.handle.net/10722/258738-
dc.description.abstractMiR-92a has been shown to be dysregulated in various cancers and exhibited differential role in carcinogenesis. In this study, we sought to delineate the functional role of miR-92a and its regulatory pathway in gastric cancer. MiR-92a expression were underexpressed in tissues of gastric cancer patients with the area under curve (AUC) of 0.78. Low expression in plasma was due to the increased promoter DNA methylation of miR-92a. Overexpression of miR-92a inhibited cell proliferation and invasion, and induced apoptosis. Furthermore, miR-92a reduced tumor growth in xenograft model. EP4 and Notch 1 were identified to be negatively regulated by miR-92a, and involved in cell growth. Moreover, NF-κB expression was inversely correlated with miR-92a in gastric cancer tissues and suppressed the expression of miR-92. This study unravels the tumor suppressive role of miR-92a involving EP4/Notch 1 signaling regulated by NF-κB in gastric cancer. Further studies on miR-92a and EP4/Notch1 may provide a new treatment strategy for gastric cancer.-
dc.languageeng-
dc.publisherImpact Journals LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html-
dc.relation.ispartofOncotarget-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectEP4-
dc.subjectNF-κB-
dc.subjectNotch1-
dc.subjectGastric cancer-
dc.subjectmiR-92-
dc.titleMiR-92 suppresses proliferation and induces apoptosis by targeting EP4/Notch 1 axis in gastric cancer-
dc.typeArticle-
dc.identifier.emailShin, VY: vyshin@hku.hk-
dc.identifier.emailSiu, JMT: jensiu@hku.hk-
dc.identifier.emailLiu, X: melx1301@hku.hk-
dc.identifier.emailNg, EKO: ngko@hku.hk-
dc.identifier.emailKwong, A: avakwong@hku.hk-
dc.identifier.emailChu, KM: chukm@hku.hk-
dc.identifier.authorityShin, VY=rp02000-
dc.identifier.authorityNg, EKO=rp01364-
dc.identifier.authorityKwong, A=rp01734-
dc.identifier.authorityChu, KM=rp00435-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.18632/oncotarget.24819-
dc.identifier.pmid29849934-
dc.identifier.pmcidPMC5966267-
dc.identifier.hkuros286624-
dc.identifier.volume9-
dc.identifier.issue36-
dc.identifier.spage24209-
dc.identifier.epage24220-
dc.publisher.placeUnited States-

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