Please use this identifier to cite or link to this item: https://doi.org/10.1038/onc.2010.504
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dc.titleAXL receptor kinase is a mediator of YAP-dependent oncogenic functions in hepatocellular carcinoma
dc.contributor.authorXu, M.Z.
dc.contributor.authorChan, S.W.
dc.contributor.authorLiu, A.M.
dc.contributor.authorWong, K.F.
dc.contributor.authorFan, S.T.
dc.contributor.authorChen, J.
dc.contributor.authorPoon, R.T.
dc.contributor.authorZender, L.
dc.contributor.authorLowe, S.W.
dc.contributor.authorHong, W.
dc.contributor.authorLuk, J.M.
dc.date.accessioned2014-11-26T09:59:28Z
dc.date.available2014-11-26T09:59:28Z
dc.date.issued2011-03-10
dc.identifier.citationXu, M.Z., Chan, S.W., Liu, A.M., Wong, K.F., Fan, S.T., Chen, J., Poon, R.T., Zender, L., Lowe, S.W., Hong, W., Luk, J.M. (2011-03-10). AXL receptor kinase is a mediator of YAP-dependent oncogenic functions in hepatocellular carcinoma. Oncogene 30 (10) : 1229-1240. ScholarBank@NUS Repository. https://doi.org/10.1038/onc.2010.504
dc.identifier.issn09509232
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/110722
dc.description.abstractYes-associated protein (YAP) is a downstream effector of the Hippo signaling pathway, which controls organ expansion and tissue development. We have recently defined the tumorigenic potential and clinical significance of the YAP1 oncogene in human hepatocellular carcinoma (HCC). The present study aims to define the tumorigenic properties of YAP in HCC and elucidate the related downstream signaling mechanism. In a gain-of-function study, we demonstrated that ectopic increased expression of YAP in the immortalized non-tumorigenic hepatocyte cell line MIHA confers tumorigenic and metastatic potentials, as evidenced by (1) enhanced aptitudes in cell viability, anchorage-independent growth, migration and invasion; (2) tumor formation in a xenograft mouse model; and (3) induction of HCC biomarker α-fetoprotein and activation of mitogen-activated protein kinase. Furthermore, we have identified AXL, a receptor tyrosine kinase, as a key downstream target that drives YAP-dependent oncogenic functions. RNAi-mediated knockdown of AXL expression decreased the ability of YAP-expressing MIHA cells and of the primary HCC cell line to proliferate and invade. These results indicate that AXL is a mediator of YAP-dependent oncogenic activities and implicates it as a potential therapeutic target for HCC. © 2011 Macmillan Publishers Limited All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1038/onc.2010.504
dc.sourceScopus
dc.subjectAXL receptor kinase
dc.subjectcancer signaling
dc.subjectHCC
dc.subjecthepatocellular carcinoma
dc.subjectHippo pathway
dc.subjectYAP1 oncogene
dc.typeArticle
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.description.doi10.1038/onc.2010.504
dc.description.sourcetitleOncogene
dc.description.volume30
dc.description.issue10
dc.description.page1229-1240
dc.description.codenONCNE
dc.identifier.isiut000288202400009
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