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RED TEMÁTICA DE INVESTIGACIÓN COOPERATIVA DEL CANCER

RD06/0020/0071

Nombre agencia financiadora Ministerio de Sanidad y Consumo
Acrónimo agencia financiadora MSC
Programa Acción Estratégica de Salud
Subprograma Articulación e Internacionalización del Sistema
Convocatoria Redes Temáticas de Investigación Cooperativa en Salud (RETICS)
Año convocatoria 2006
Unidad de gestión Subdirección General de Redes y Centros de Investigación Cooperativa
Centro beneficiario FUNDACIÓN PARA LA INVESTIGACIÓN MÉDICA APLICADA (FIMA)
Centro realización FUNDACION PARA LA INVESTIGACION MEDICA APLICADA
Identificador persistente No disponible

Publicaciones

Resultados totales (Incluyendo duplicados): 1
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EVI1 controls proliferation in acute myeloid leukaemia through modulation of miR-1-2

Academica-e. Repositorio Institucional de la Universidad Pública de Navarra
  • Gómez-Benito, María
  • Conchillo, Ana
  • García, M. A.
  • Vázquez Urio, Iria
  • Maicas, Miren
  • Vicente, Carmen
  • Cristóbal, Ion
  • Marcotegui, Nerea
  • García-Ortí, L.
  • Bandrés Elizalde, Eva
  • Calasanz, María José
  • Alonso, M. M.
  • Odero, María D.
Acceso cerrado a este documento. No se encuentra disponible para la consulta pública. Depositado en Academica-e para cumplir con los requisitos de evaluación y acreditación académica del autor/a (sexenios, acreditaciones, etc.)., Bakground: the EVI1(ecotropic virus integration site 1) gene codes for a zinc-finger transcription factor, whose transcriptional activation leads to a particularly aggressive form of acute myeloid leukaemia (AML). Although, EVI1 interactions with key proteins in hematopoiesis have been previously described, the precise role of this transcription factor in promoting leukaemic transformation is not completely understood. Recent works have identified specific microRNA (miRNA) signatures in different AML subgroups. However, there is no analysis of miRNAs profiles associated with EVI1 overexpression in humans. Methods: we performed QT-RT-PCR to assess the expression of 250 miRNAs in cell lines with or without EVI1 overexpression and in patient samples. We used ChIP assays to evaluated the possible binding of EVI1 binding to the putative miRNA promoter. Proliferation of the different cell lines transfected with the anti- or pre-miRs was quantified by MTT. Results: our data showed that EVI1 expression was significantly correlated with the expression of miR-1-2 and miR-133-a-1 in established cell lines and in patient samples. ChIP assays confirmed that EVI1 binds directly to the promoter of these two miRNAs. However, only miR-1-2 was involved in abnormal proliferation in EVI1 expressing cell lines. Conclusions: our data showed that EVI1 controls proliferation in AML through modulation of miR-1-2. This study contributes to further understand the transcriptional networks involving transcription factors and miRNAs in AML., This work was supported by Ministerio de Salud (FIS-CD07/00045), Ministerio de Educación y Ciencia (SAF2005/06425), Ministerio de Ciencia e Innovación (PI081687), ISCIII-RETIC (RD06/0020/0078 and RD06/0020/0071), Departamento Salud del Gobierno de Navarra (14/2008), and Fundació para la Investigación Médica Aplicada y UTE (Spain).