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Genomic and epigenomic EBF1 alterations modulate TERT expression in gastric cancer.
Xing, Manjie; Ooi, Wen Fong; Tan, Jing; Qamra, Aditi; Lee, Po-Hsien; Li, Zhimei; Xu, Chang; Padmanabhan, Nisha; Lim, Jing Quan; Guo, Yu Amanda; Yao, Xiaosai; Amit, Mandoli; Ng, Ley Moy; Sheng, Taotao; Wang, Jing; Huang, Kie Kyon; Anene-Nzelu, Chukwuemeka George; Ho, Shamaine Wei Ting; Ray, Mohana; Ma, Lijia; Fazzi, Gregorio; Lim, Kevin Junliang; Wijaya, Giovani Claresta; Zhang, Shenli; Nandi, Tannistha; Yan, Tingdong; Chang, Mei Mei; Das, Kakoli; Isa, Zul Fazreen Adam; Wu, Jeanie; Poon, Polly Suk Yean; Lam, Yue Ning; Lin, Joyce Suling; Tay, Su Ting; Lee, Ming Hui; Tan, Angie Lay Keng; Ong, Xuewen; White, Kevin; Rozen, Steven George; Beer, Michael; Foo, Roger Sik Yin; Grabsch, Heike Irmgard; Skanderup, Anders Jacobsen; Li, Shang; Teh, Bin Tean; Tan, Patrick.
Afiliación
  • Xing M; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Ooi WF; Cancer Therapeutics and Stratified Oncology, Genome Institute of Singapore, Singapore.
  • Tan J; NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore.
  • Qamra A; Cancer Therapeutics and Stratified Oncology, Genome Institute of Singapore, Singapore.
  • Lee PH; State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, China.
  • Li Z; Laboratory of Cancer Epigenome, Department of Medical Sciences, National Cancer Centre, Singapore.
  • Xu C; Cancer Therapeutics and Stratified Oncology, Genome Institute of Singapore, Singapore.
  • Padmanabhan N; NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, Singapore.
  • Lim JQ; Cancer Science Institute of Singapore, National University of Singapore, Singapore.
  • Guo YA; Laboratory of Cancer Epigenome, Department of Medical Sciences, National Cancer Centre, Singapore.
  • Yao X; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Amit M; Cancer Science Institute of Singapore, National University of Singapore, Singapore.
  • Ng LM; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Sheng T; Lymphoma Genomic Translational Research Laboratory, Cellular and Molecular Research, National Cancer Centre Singapore, Singapore.
  • Wang J; Computational and Systems Biology, Agency for Science Technology and Research, Genome Institute of Singapore.
  • Huang KK; Institute of Molecular and Cell Biology, Singapore.
  • Anene-Nzelu CG; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Ho SWT; Cancer Science Institute of Singapore, National University of Singapore, Singapore.
  • Ray M; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Ma L; Department of Biochemistry, National University of Singapore, Singapore.
  • Fazzi G; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Lim KJ; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Wijaya GC; Cardiovascular Research Institute, National University Health System, Singapore.
  • Zhang S; Human Genetics, Genome Institute of Singapore, Singapore.
  • Nandi T; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Yan T; Cancer Science Institute of Singapore, National University of Singapore, Singapore.
  • Chang MM; Institute for Genomics and Systems Biology, University of Chicago, Chicago, Illinois, USA.
  • Das K; Institute for Genomics and Systems Biology, University of Chicago, Chicago, Illinois, USA.
  • Isa ZFA; Department of Pathology, GROW School for Oncology and Developmental Biology, Maastricht University Medical Center, Maastricht, Netherlands.
  • Wu J; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Poon PSY; Laboratory of Cancer Epigenome, Department of Medical Sciences, National Cancer Centre, Singapore.
  • Lam YN; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Lin JS; Cancer Therapeutics and Stratified Oncology, Genome Institute of Singapore, Singapore.
  • Tay ST; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Lee MH; Computational and Systems Biology, Agency for Science Technology and Research, Genome Institute of Singapore.
  • Tan ALK; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Ong X; Cancer Therapeutics and Stratified Oncology, Genome Institute of Singapore, Singapore.
  • White K; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Rozen SG; Cancer Therapeutics and Stratified Oncology, Genome Institute of Singapore, Singapore.
  • Beer M; Cancer Therapeutics and Stratified Oncology, Genome Institute of Singapore, Singapore.
  • Foo RSY; Cancer Therapeutics and Stratified Oncology, Genome Institute of Singapore, Singapore.
  • Grabsch HI; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Skanderup AJ; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Li S; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Teh BT; Cancer and Stem Cell Biology Program, Duke-NUS Medical School, Singapore.
  • Tan P; Institute for Genomics and Systems Biology, University of Chicago, Chicago, Illinois, USA.
J Clin Invest ; 130(6): 3005-3020, 2020 06 01.
Article en En | MEDLINE | ID: mdl-32364535
Transcriptional reactivation of telomerase catalytic subunit (TERT) is a frequent hallmark of cancer, occurring in 90% of human malignancies. However, specific mechanisms driving TERT reactivation remain obscure for many tumor types and in particular gastric cancer (GC), a leading cause of global cancer mortality. Here, through comprehensive genomic and epigenomic analysis of primary GCs and GC cell lines, we identified the transcription factor early B cell factor 1 (EBF1) as a TERT transcriptional repressor and inactivation of EBF1 function as a major cause of TERT upregulation. Abolishment of EBF1 function occurs through 3 distinct (epi)genomic mechanisms. First, EBF1 is epigenetically silenced via DNA methyltransferase, polycomb-repressive complex 2 (PRC2), and histone deacetylase activity in GCs. Second, recurrent, somatic, and heterozygous EBF1 DNA-binding domain mutations result in the production of dominant-negative EBF1 isoforms. Third, more rarely, genomic deletions and rearrangements proximal to the TERT promoter remobilize or abolish EBF1-binding sites, derepressing TERT and leading to high TERT expression. EBF1 is also functionally required for various malignant phenotypes in vitro and in vivo, highlighting its importance for GC development. These results indicate that multimodal genomic and epigenomic alterations underpin TERT reactivation in GC, converging on transcriptional repressors such as EBF1.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Gástricas / Regulación Enzimológica de la Expresión Génica / Regulación Neoplásica de la Expresión Génica / Transactivadores / Telomerasa / Epigenómica / Proteínas de Neoplasias Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: J Clin Invest Año: 2020 Tipo del documento: Article País de afiliación: Singapur Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Gástricas / Regulación Enzimológica de la Expresión Génica / Regulación Neoplásica de la Expresión Génica / Transactivadores / Telomerasa / Epigenómica / Proteínas de Neoplasias Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: J Clin Invest Año: 2020 Tipo del documento: Article País de afiliación: Singapur Pais de publicación: Estados Unidos