Matches in SemOpenAlex for { <https://semopenalex.org/work/W2728934905> ?p ?o ?g. }
- W2728934905 endingPage "63120" @default.
- W2728934905 startingPage "63110" @default.
- W2728934905 abstract "// Yin-Cheng Huang 1, 2, * , Sheng-Jia Lin 3, * , Hung-Yu Shih 3 , Chung-Han Chou 4 , Hsiao-Han Chu 4 , Ching-Chi Chiu 5 , Chiou-Hwa Yuh 6 , Tu-Hsueh Yeh 5, 7, 8 and Yi-Chuan Cheng 3, 5 1 College of Medicine, Chang Gung University, Taoyuan, Taiwan 2 Department of Neurosurgery, Chang Gung Memorial Hospital at Linkou Medical Center, Taoyuan, Taiwan 3 Graduate Institute of Biomedical Sciences, College of Medicine, Chang-Gung University, Taoyuan, Taiwan 4 School of Medicine, College of Medicine, Chang-Gung University, Taoyuan, Taiwan 5 Neuroscience Research Center, Chang Gung Memorial Hospital at Linkou Medical Center, Taoyuan, Taiwan 6 Institute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan 7 Department of Neurology, Taipei Medical University Hospital, Taipei, Taiwan 8 School of Medicine, Taipei Medical University, Taipei, Taiwan * Co-first authors Correspondence to: Yi-Chuan Cheng, email: yccheng@mail.cgu.edu.tw Tu-Hsueh Yeh, email: neuroyeh@gmail.com Keywords: KMT2A, NOTCH, glioma, zebrafish Received: August 05, 2016 Accepted: May 22, 2017 Published: June 27, 2017 ABSTRACT Glioblastomas are among the most fatal brain tumors; however, the molecular determinants of their tumorigenic behavior are not adequately defined. In this study, we analyzed the role of KMT2A in the glioblastoma cell line U-87 MG. KMT2A knockdown promoted cell proliferation. Moreover, it increased the DNA methylation of NOTCH1 and NOTCH3 and reduced the expression of NOTCH1 and NOTCH3 . NOTCH1 or NOTCH3 activation inhibited U-87 MG cell proliferation, whereas NOTCH1 and NOTCH3 inhibition by shRNAs induced cell proliferation, thus demonstrating the tumor-suppressive ability of NOTCH1 and NOTCH3 in U-87 MG cells. The induced cell proliferation caused by KMT2A knockdown could be nullified by using either constitutively active NOTCH1 or constitutively active NOTCH3. This result demonstrates that KMT2A positively regulates NOTCH1 and NOTCH3 and that this mechanism is essential for inhibiting the U-87 MG cell proliferation. The role of KMT2A knockdown in promoting tumor growth was further confirmed in vivo by transplanting U-87 MG cells into the brains of zebrafish larvae. In conclusion, we identified KMT2A-NOTCH as a negative regulatory cascade for glioblastoma cell proliferation, and this result provides important information for KMT2A- or NOTCH-targeted therapeutic strategies for brain tumors." @default.
- W2728934905 created "2017-07-14" @default.
- W2728934905 creator A5009510828 @default.
- W2728934905 creator A5013225939 @default.
- W2728934905 creator A5013421581 @default.
- W2728934905 creator A5018969206 @default.
- W2728934905 creator A5019729860 @default.
- W2728934905 creator A5030172482 @default.
- W2728934905 creator A5034363174 @default.
- W2728934905 creator A5038674737 @default.
- W2728934905 creator A5086404151 @default.
- W2728934905 date "2017-06-27" @default.
- W2728934905 modified "2023-09-25" @default.
- W2728934905 title "Epigenetic regulation of NOTCH1 and NOTCH3 by KMT2A inhibits glioma proliferation" @default.
- W2728934905 cites W1500946936 @default.
- W2728934905 cites W1583158213 @default.
- W2728934905 cites W1591554430 @default.
- W2728934905 cites W1875559588 @default.
- W2728934905 cites W1975636865 @default.
- W2728934905 cites W1985171686 @default.
- W2728934905 cites W1992048312 @default.
- W2728934905 cites W1997879666 @default.
- W2728934905 cites W1999684691 @default.
- W2728934905 cites W2013359619 @default.
- W2728934905 cites W2015346961 @default.
- W2728934905 cites W2016024994 @default.
- W2728934905 cites W2016058704 @default.
- W2728934905 cites W2022495797 @default.
- W2728934905 cites W2027711745 @default.
- W2728934905 cites W2038570555 @default.
- W2728934905 cites W2041440766 @default.
- W2728934905 cites W2049449372 @default.
- W2728934905 cites W2057224174 @default.
- W2728934905 cites W2057672963 @default.
- W2728934905 cites W2057927546 @default.
- W2728934905 cites W2061740109 @default.
- W2728934905 cites W2077654571 @default.
- W2728934905 cites W2080365007 @default.
- W2728934905 cites W2082592723 @default.
- W2728934905 cites W2082694975 @default.
- W2728934905 cites W2085092579 @default.
- W2728934905 cites W2098769593 @default.
- W2728934905 cites W2099705390 @default.
- W2728934905 cites W2108333200 @default.
- W2728934905 cites W2108373725 @default.
- W2728934905 cites W2113811233 @default.
- W2728934905 cites W2123349002 @default.
- W2728934905 cites W2133977960 @default.
- W2728934905 cites W2143973426 @default.
- W2728934905 cites W2159833518 @default.
- W2728934905 cites W2162184748 @default.
- W2728934905 cites W2163542527 @default.
- W2728934905 cites W2163686060 @default.
- W2728934905 cites W2163798887 @default.
- W2728934905 cites W2165119870 @default.
- W2728934905 cites W2181996073 @default.
- W2728934905 cites W2182620097 @default.
- W2728934905 cites W2192601036 @default.
- W2728934905 cites W2248210411 @default.
- W2728934905 cites W2465761834 @default.
- W2728934905 cites W4238448376 @default.
- W2728934905 doi "https://doi.org/10.18632/oncotarget.18668" @default.
- W2728934905 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5609907" @default.
- W2728934905 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28968975" @default.
- W2728934905 hasPublicationYear "2017" @default.
- W2728934905 type Work @default.
- W2728934905 sameAs 2728934905 @default.
- W2728934905 citedByCount "20" @default.
- W2728934905 countsByYear W27289349052018 @default.
- W2728934905 countsByYear W27289349052019 @default.
- W2728934905 countsByYear W27289349052020 @default.
- W2728934905 countsByYear W27289349052021 @default.
- W2728934905 countsByYear W27289349052022 @default.
- W2728934905 countsByYear W27289349052023 @default.
- W2728934905 crossrefType "journal-article" @default.
- W2728934905 hasAuthorship W2728934905A5009510828 @default.
- W2728934905 hasAuthorship W2728934905A5013225939 @default.
- W2728934905 hasAuthorship W2728934905A5013421581 @default.
- W2728934905 hasAuthorship W2728934905A5018969206 @default.
- W2728934905 hasAuthorship W2728934905A5019729860 @default.
- W2728934905 hasAuthorship W2728934905A5030172482 @default.
- W2728934905 hasAuthorship W2728934905A5034363174 @default.
- W2728934905 hasAuthorship W2728934905A5038674737 @default.
- W2728934905 hasAuthorship W2728934905A5086404151 @default.
- W2728934905 hasBestOaLocation W27289349051 @default.
- W2728934905 hasConcept C104317684 @default.
- W2728934905 hasConcept C126322002 @default.
- W2728934905 hasConcept C143998085 @default.
- W2728934905 hasConcept C150194340 @default.
- W2728934905 hasConcept C173396325 @default.
- W2728934905 hasConcept C190283241 @default.
- W2728934905 hasConcept C190727270 @default.
- W2728934905 hasConcept C41091548 @default.
- W2728934905 hasConcept C502942594 @default.
- W2728934905 hasConcept C54355233 @default.
- W2728934905 hasConcept C62112901 @default.
- W2728934905 hasConcept C71924100 @default.
- W2728934905 hasConcept C86803240 @default.