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 Blood, 8 January 2009, Vol. 113, No. 2, pp. 412-421.
Prepublished online as a Blood First Edition Paper on October 21, 2008; DOI 10.1182/blood-2008-05-158139.

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Submitted May 21, 2008
Accepted September 30, 2008

Transcriptional repression of microRNA genes by PML-RARA increases expression of key cancer proteins in acute promyelocytic leukemia

Anne Saumet, Guillaume Vetter, Manuella Bouttier, Elodie Portales-Casamar, Wyeth W. Wasserman, Thomas Maurin, Bernard Mari, Pascal Barbry, Laurent Vallar, Evelyne Friederich, Khalil Arar, Bruno Cassinat, Christine Chomienne, and Charles-Henri Lecellier*

Institut de Genetique Humaine, CNRS UPR1142, Montpellier, France
Universite du Luxembourg, Luxembourg, Luxembourg
Institut de Genetique Moleculaire de Montpellier, CNRS UMR5535-IFR122, Montpellier, France
University of British Columbia, Vancouver, BC, Canada
Institut de Pharmacologie Moleculaire et Cellulaire, UMR6097 CNRS/UNSA, Sophia Antipolis, France
CRP-Sante, Luxembourg, Luxembourg
Sigma-Proligo, Evry, France
Institut Universitaire d'Hematologie, Hopital Saint-Louis, INSERM U718, Paris, France

* Corresponding author; email: charles.lecellier{at}igmm.cnrs.fr.

Micro(mi)RNAs are small non-coding RNAs that orchestrate many key aspects of cell physiology and their deregulation are often linked to distinct diseases including cancer. Here, we studied the contribution of miRNAs in a well characterized human myeloid leukemia, Acute Promyelocytic Leukemia (APL), targeted by retinoic acid and trioxide arsenic therapy. We identified several miRNAs transcriptionally repressed by the APL-associated PML-RAR oncogene which are released after treatment with all-trans retinoic acid. These co-regulated miRNAs were found to control, in a coordinated manner, crucial pathways linked to leukemogenesis, such as HOX proteins and cell adhesion molecules whose expressions are thereby repressed by the chemotherapy. Thus, APL appears linked to transcriptional perturbation of miRNA genes and clinical protocols able to successfully eradicate cancer cells may do so by restoring miRNA expression. The identification of abnormal miRNA biogenesis in cancer may therefore provide novel biomarkers and therapeutic targets in myeloid leukemias.


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