Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.febslet.2011.05.042
DC FieldValue
dc.titleMiR-198 inhibits migration and invasion of hepatocellular carcinoma cells by targeting the HGF/c-MET pathway
dc.contributor.authorTan, S.
dc.contributor.authorLi, R.
dc.contributor.authorDing, K.
dc.contributor.authorLobie, P.E.
dc.contributor.authorZhu, T.
dc.date.accessioned2014-11-26T07:46:11Z
dc.date.available2014-11-26T07:46:11Z
dc.date.issued2011-07-21
dc.identifier.citationTan, S., Li, R., Ding, K., Lobie, P.E., Zhu, T. (2011-07-21). MiR-198 inhibits migration and invasion of hepatocellular carcinoma cells by targeting the HGF/c-MET pathway. FEBS Letters 585 (14) : 2229-2234. ScholarBank@NUS Repository. https://doi.org/10.1016/j.febslet.2011.05.042
dc.identifier.issn00145793
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/109468
dc.description.abstractMetastasis is the leading cause of death in patients with hepatocellular carcinoma (HCC) and microRNAs have been implicated to influence this process. Emerging evidence indicates that miR-198 is down-regulated in HCC compared to normal liver parenchyma, but the functional roles of miR-198 in HCC cells remains unexplored. Herein, we show that miR-198 directly targets c-MET via its 3′UTR. Forced expression of miR-198 decreased c-MET expression at both mRNA and protein levels and consequently diminished HGF induced phosphorylation of p44/42 MAPK in HCC cells. Forced expression of miR-198 inhibited HGF promotion of HCC cell migration and invasion in a c-MET dependent manner. In conclusion, we have identified miR-198 as a novel suppressor of HCC cell invasion by negative regulation of the HGF/c-MET pathway. © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.febslet.2011.05.042
dc.sourceScopus
dc.subjectc-MET
dc.subjectHepatocellular carcinoma
dc.subjectInvasion
dc.subjectmiR-198
dc.typeArticle
dc.contributor.departmentPHARMACOLOGY
dc.description.doi10.1016/j.febslet.2011.05.042
dc.description.sourcetitleFEBS Letters
dc.description.volume585
dc.description.issue14
dc.description.page2229-2234
dc.description.codenFEBLA
dc.identifier.isiut000292772800016
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