Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/80288
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dc.contributorDepartment of Applied Biology and Chemical Technology-
dc.creatorChan, LH-
dc.creatorZhou, L-
dc.creatorNg, KY-
dc.creatorWong, TL-
dc.creatorLee, TK-
dc.creatorSharma, R-
dc.creatorLoong, JH-
dc.creatorChing, YP-
dc.creatorYuan, YF-
dc.creatorXie, D-
dc.creatorLo, CM-
dc.creatorMan, K-
dc.creatorArtegiani, B-
dc.creatorClevers, H-
dc.creatorYan, HH-
dc.creatorLeung, SY-
dc.creatorRichard, S-
dc.creatorGuan, XY-
dc.creatorHuen, MSY-
dc.creatorMa, S-
dc.date.accessioned2019-01-30T09:14:40Z-
dc.date.available2019-01-30T09:14:40Z-
dc.identifier.urihttp://hdl.handle.net/10397/80288-
dc.language.isoenen_US
dc.publisherCell Pressen_US
dc.rights© 2018 The Author(s).en_US
dc.rightsThis is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).en_US
dc.rightsThe following publication Chan, L.H., Zhou, L., Ng, K.Y., Wong, T.L., Lee, T.K., Sharma, R., ... & Ma, S. (2018). PRMT6 regulates RAS/RAF binding and MEK/ERK-Mediated cancer sternness activities in hepatocellular carcinoma through CRAF methylation. Cell reports, 25 (3), 690-701 is available at https://dx.doi.org/10.1016/j.celrep.2018.09.053en_US
dc.titlePRMT6 regulates RAS/RAF binding and MEK/ERK-Mediated cancer sternness activities in hepatocellular carcinoma through CRAF methylationen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage690-
dc.identifier.epage701-
dc.identifier.volume25-
dc.identifier.issue3-
dc.identifier.doi10.1016/j.celrep.2018.09.053-
dcterms.abstractArginine methylation is a post-translational modification that plays pivotal roles in signal transduction and gene transcription during cell fate determination. We found protein methyltransferase 6 (PRMT6) to be frequently downregulated in hepatocellular carcinoma (HCC) and its expression to negatively correlate with aggressive cancer features in HCC patients. Silencing of PRMT6 promoted the tumor-initiating, metastasis, and therapy resistance potential of HCC cell lines and patient-derived organoids. Consistently, loss of PRMT6 expression aggravated liver tumorigenesis in a chemical-induced HCC PRMT6 knockout (PRMT6(-/-)) mouse model. Integrated transcriptome and protein-protein interaction studies revealed an enrichment of genes implicated in RAS signaling and showed that PRMT6 interacted with CRAF on arginine 100, which decreased its RAS binding potential and altered its downstream MEK/ERK signaling. Our work describes a critical repressive function for PRMT6 in maintenance of HCC cells by regulating RAS binding and MEK/ERK signaling via methylation of CRAF on arginine 100.-
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationCell reports, Oct. 2018, v. 25, no. 3, p. 690-701-
dcterms.isPartOfCell reports-
dcterms.issued2018-
dc.identifier.isiWOS:000448217500014-
dc.identifier.scopus2-s2.0-85054755052-
dc.identifier.pmid30332648-
dc.identifier.eissn2211-1247-
dc.description.validate201901 bcrc-
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumberOA_IR/PIRAen_US
dc.description.pubStatusPublisheden_US
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