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Long Noncoding RNA PURPL Suppresses Basal p53 Levels and Promotes Tumorigenicity in Colorectal Cancer.
Li, Xiao Ling; Subramanian, Murugan; Jones, Matthew F; Chaudhary, Ritu; Singh, Deepak K; Zong, Xinying; Gryder, Berkley; Sindri, Sivasish; Mo, Min; Schetter, Aaron; Wen, Xinyu; Parvathaneni, Swetha; Kazandjian, Dickran; Jenkins, Lisa M; Tang, Wei; Elloumi, Fathi; Martindale, Jennifer L; Huarte, Maite; Zhu, Yuelin; Robles, Ana I; Frier, Susan M; Rigo, Frank; Cam, Maggie; Ambs, Stefan; Sharma, Sudha; Harris, Curtis C; Dasso, Mary; Prasanth, Kannanganattu V; Lal, Ashish.
Afiliação
  • Li XL; Regulatory RNAs and Cancer Section, Genetics Branch, Center for Cancer Research (CCR), National Cancer Institute (NCI), NIH, Bethesda, MD 20892, USA.
  • Subramanian M; Regulatory RNAs and Cancer Section, Genetics Branch, Center for Cancer Research (CCR), National Cancer Institute (NCI), NIH, Bethesda, MD 20892, USA.
  • Jones MF; Regulatory RNAs and Cancer Section, Genetics Branch, Center for Cancer Research (CCR), National Cancer Institute (NCI), NIH, Bethesda, MD 20892, USA.
  • Chaudhary R; Regulatory RNAs and Cancer Section, Genetics Branch, Center for Cancer Research (CCR), National Cancer Institute (NCI), NIH, Bethesda, MD 20892, USA.
  • Singh DK; Department of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
  • Zong X; Department of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
  • Gryder B; Oncogenomics Section, Genetics Branch, CCR, NCI, NIH, Bethesda, MD 20892, USA.
  • Sindri S; Oncogenomics Section, Genetics Branch, CCR, NCI, NIH, Bethesda, MD 20892, USA.
  • Mo M; Laboratory of Gene Regulation and Development, National Institute of Child Health and Human Development, NIH, Bethesda, MD 20892, USA.
  • Schetter A; Molecular Genetics and Carcinogenesis Section, Laboratory of Human Carcinogenesis, CCR, NCI, NIH, Bethesda, MD 20892, USA.
  • Wen X; Oncogenomics Section, Genetics Branch, CCR, NCI, NIH, Bethesda, MD 20892, USA.
  • Parvathaneni S; Department of Biochemistry and Molecular Biology, College of Medicine, Howard University, Washington, DC 20059, USA.
  • Kazandjian D; Molecular Genetics and Carcinogenesis Section, Laboratory of Human Carcinogenesis, CCR, NCI, NIH, Bethesda, MD 20892, USA.
  • Jenkins LM; Laboratory of Cell Biology, CCR, NCI, NIH, Bethesda, MD 20892, USA.
  • Tang W; Molecular Epidemiology Section, Laboratory of Human Carcinogenesis, CCR, NCI, NIH, Bethesda, MD 20892, USA.
  • Elloumi F; Office of Science and Technology Resources, CCR, NCI, NIH, Bethesda, MD 20892, USA.
  • Martindale JL; Laboratory of Genetics, National Institute on Aging-Intramural Research Program, NIH, Baltimore, MD 21224, USA.
  • Huarte M; Center for Applied Medical Research, Department of Gene Therapy and Regulation of Gene Expression, University of Navarra, 31008 Pamplona, Spain.
  • Zhu Y; Molecular Genetics Section, Genetics Branch, CCR, NCI, NIH, Bethesda, MD 28092, USA.
  • Robles AI; Molecular Genetics and Carcinogenesis Section, Laboratory of Human Carcinogenesis, CCR, NCI, NIH, Bethesda, MD 20892, USA.
  • Frier SM; Ionis Pharmaceuticals, Carlsbad, CA 92010, USA.
  • Rigo F; Ionis Pharmaceuticals, Carlsbad, CA 92010, USA.
  • Cam M; Office of Science and Technology Resources, CCR, NCI, NIH, Bethesda, MD 20892, USA.
  • Ambs S; Molecular Epidemiology Section, Laboratory of Human Carcinogenesis, CCR, NCI, NIH, Bethesda, MD 20892, USA.
  • Sharma S; Department of Biochemistry and Molecular Biology, College of Medicine, Howard University, Washington, DC 20059, USA.
  • Harris CC; Molecular Genetics and Carcinogenesis Section, Laboratory of Human Carcinogenesis, CCR, NCI, NIH, Bethesda, MD 20892, USA.
  • Dasso M; Laboratory of Gene Regulation and Development, National Institute of Child Health and Human Development, NIH, Bethesda, MD 20892, USA.
  • Prasanth KV; Department of Cell and Developmental Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
  • Lal A; Regulatory RNAs and Cancer Section, Genetics Branch, Center for Cancer Research (CCR), National Cancer Institute (NCI), NIH, Bethesda, MD 20892, USA. Electronic address: ashish.lal@nih.gov.
Cell Rep ; 20(10): 2408-2423, 2017 Sep 05.
Article em En | MEDLINE | ID: mdl-28877474
ABSTRACT
Basal p53 levels are tightly suppressed under normal conditions. Disrupting this regulation results in elevated p53 levels to induce cell cycle arrest, apoptosis, and tumor suppression. Here, we report the suppression of basal p53 levels by a nuclear, p53-regulated long noncoding RNA that we termed PURPL (p53 upregulated regulator of p53 levels). Targeted depletion of PURPL in colorectal cancer cells results in elevated basal p53 levels and induces growth defects in cell culture and in mouse xenografts. PURPL associates with MYBBP1A, a protein that binds to and stabilizes p53, and inhibits the formation of the p53-MYBBP1A complex. In the absence of PURPL, MYBBP1A interacts with and stabilizes p53. Silencing MYBBP1A significantly rescues basal p53 levels and proliferation in PURPL-deficient cells, suggesting that MYBBP1A mediates the effect of PURPL in regulating p53. These results reveal a p53-PURPL auto-regulatory feedback loop and demonstrate a role for PURPL in maintaining basal p53 levels.
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Texto completo: 1 Coleções: 01-internacional Contexto em Saúde: 6_ODS3_enfermedades_notrasmisibles Base de dados: MEDLINE Assunto principal: Neoplasias Colorretais / Proteína Supressora de Tumor p53 / RNA Longo não Codificante Limite: Humans Idioma: En Revista: Cell Rep Ano de publicação: 2017 Tipo de documento: Article
Texto completo
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XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Contexto em Saúde: 6_ODS3_enfermedades_notrasmisibles Base de dados: MEDLINE Assunto principal: Neoplasias Colorretais / Proteína Supressora de Tumor p53 / RNA Longo não Codificante Limite: Humans Idioma: En Revista: Cell Rep Ano de publicação: 2017 Tipo de documento: Article