Specific inhibition of bcr-abl gene expression by small interfering RNA

DOI PDF 被引用文献8件
  • Michaela Scherr
    From the Department of Hematology and Oncology, Hannover Medical School, Germany; and the Department of Molecular Biology, University of Tübingen, Germany.
  • Karin Battmer
    From the Department of Hematology and Oncology, Hannover Medical School, Germany; and the Department of Molecular Biology, University of Tübingen, Germany.
  • Thomas Winkler
    From the Department of Hematology and Oncology, Hannover Medical School, Germany; and the Department of Molecular Biology, University of Tübingen, Germany.
  • Olaf Heidenreich
    From the Department of Hematology and Oncology, Hannover Medical School, Germany; and the Department of Molecular Biology, University of Tübingen, Germany.
  • Arnold Ganser
    From the Department of Hematology and Oncology, Hannover Medical School, Germany; and the Department of Molecular Biology, University of Tübingen, Germany.
  • Matthias Eder
    From the Department of Hematology and Oncology, Hannover Medical School, Germany; and the Department of Molecular Biology, University of Tübingen, Germany.

抄録

<jats:p>Small interfering RNAs (siRNAs) were designed to target thebcr-abl oncogene, which causes chronic myeloid leukemia (CML) and bcr-abl–positive acute lymphoblastic leukemia (ALL). Chemically synthesized anti–bcr-abl siRNAs were selected using reporter gene constructs and were found to reduce bcr-abl mRNA up to 87% in bcr-abl–positive cell lines and in primary cells from CML patients. This mRNA reduction was specific for bcr-abl because c-abl and c-bcr mRNA levels remained unaffected. Furthermore, protein expression of BCR-ABL and of laminA/C was reduced by specific siRNAs up to 80% in bcr-abl–positive and normal CD34+ cells, respectively. Finally, anti–bcr-abl siRNA inhibited BCR-ABL–dependent, but not cytokine-dependent, proliferation in a bcr-abl–positive cell line. These data demonstrate that siRNA can specifically and efficiently interfere with the expression of an oncogenic fusion gene in hematopoietic cells.</jats:p>

収録刊行物

  • Blood

    Blood 101 (4), 1566-1569, 2003-02-15

    American Society of Hematology

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