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dc.contributor.authorKAUSHIKNEHA-
dc.date.accessioned2019-12-06T05:32:17Z-
dc.date.available2019-12-06T05:32:17Z-
dc.date.issued2018-03-
dc.identifier.citationARTIFICIAL CELLS NANOMEDICINE AND BIOTECHNOLOGY, v. 46, page. 87-95, Supplement:2en_US
dc.identifier.issn2169-1401-
dc.identifier.issn2169-141X-
dc.identifier.urihttps://www.tandfonline.com/doi/full/10.1080/21691401.2018.1452022-
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/117891-
dc.description.abstractReceptor tyrosine kinase Mer (MerTK) has been shown to be highly expressed in Glioblastoma multiforme (GBM) in comparison to its healthy counterpart and is implicated in brain tumorigenesis. Clarifying the underlying mechanism of MerTK induced invasiveness would result in novel strategies to improve patient's response to chemotherapeutics. In vitro and in vivo assays were performed to examine the functional role of cancer stem sell (CSC) maintenance in MerTK associated invasiveness. In this article, we demonstrate that apart from GBM cells, MerTK is also upregulated in GBM stem-like cells and associated with an increased infiltrative potential of brain tumors in vivo. Silencing of MerTK suppressed the self-renewal of patient-derived GBM stem-like cells. The signaling mechanisms by which MerTK contributes to CSC maintenance have largely been obscure. Molecular analyses revealed that high expression of the signal transducer and activator of transcription 3 (STAT3)- Kirsten rat sarcoma viral oncogene homolog (KRAS) and proto-oncogene tyrosine-protein kinase SRC axis supports MerTK-induced CSC maintenance in GBM spheroids. Furthermore, a short-hairpin RNA-mediated MerTK knockdown effectively blocked invasiveness and N-cadherin expression in mouse xenografts. Collectively, our results uncover a critical function of MerTK in CSC maintenance. Considering the low basal level of MerTK expression in healthy brain cells, evaluation of MerTK as a therapeutic target should advance the research into better therapeutics for GBM.en_US
dc.description.sponsorshipThis work was supported by the National Research Foundation (NRF) and Ministry of Science, ICT and Future Planning, Korean Government, through its National Nuclear Technology Program [NRF-2015M2A2A7A01044998 and NRF-2016R1C1B2010851].en_US
dc.language.isoen_USen_US
dc.publisherTAYLOR & FRANCIS LTDen_US
dc.subjectMerTKen_US
dc.subjectself-renewalen_US
dc.subjectKRASen_US
dc.subjectSTAT3en_US
dc.subjectSRCen_US
dc.titleMerTK mediates STAT3–KRAS/SRC-signaling axis for glioma stem cell maintenanceen_US
dc.typeArticleen_US
dc.identifier.doi10.1080/21691401.2018.1452022-
dc.relation.page1-9-
dc.relation.journalARTIFICIAL CELLS NANOMEDICINE AND BIOTECHNOLOGY-
dc.contributor.googleauthorEom, Hyojin-
dc.contributor.googleauthorKaushik, Neha-
dc.contributor.googleauthorYoo, Ki-Chun-
dc.contributor.googleauthorShim, Jin-Kyoung-
dc.contributor.googleauthorKwon, Munjin-
dc.contributor.googleauthorChoi, Mi-Young-
dc.contributor.googleauthorYoon, Taeyoung-
dc.contributor.googleauthorKang, Seok-Gu-
dc.contributor.googleauthorLee, Su-Jae-
dc.relation.code2018001957-
dc.sector.campusS-
dc.sector.daehakRESEARCH INSTITUTE[S]-
dc.sector.departmentTHE RESEARCH INSTITUTE FOR NATURAL SCIENCES-
dc.identifier.pidneha1987-
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