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 Blood, 5 November 2009, Vol. 114, No. 19, pp. 4169-4178.
Prepublished online as a Blood First Edition Paper on September 11, 2009; DOI 10.1182/blood-2008-12-191619.

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LYMPHOID NEOPLASIA

miR-128b is a potent glucocorticoid sensitizer in MLL-AF4 acute lymphocytic leukemia cells and exerts cooperative effects with miR-221

Ai Kotani1,2, Daon Ha3, James Hsieh4, Prakash K. Rao1, Diana Schotte5, Monique L. den Boer5, Scott A. Armstrong6, and Harvey F. Lodish1,3

1 Whitehead Institute for Biomedical Research, Cambridge, MA; 2 Division of Molecular Therapy Advanced Clinical Research Center Institute of Medical Science, University of Tokyo, Tokyo, Japan; 3 Department of Biology, Massachusetts Institute of Technology, Cambridge; 4 Molecular Oncology, Department of Medicine, Siteman Cancer Center, Washington University School of Medicine, St Louis, MO; 5 Department of Pediatric Oncology/Hematology, Erasmus MC/Sophia Children's Hospital, Rotterdam, The Netherlands; and 6 Division of Hematology/Oncology, Children's Hospital and Harvard Medical School, Boston, MA

MLL-AF4 acute lymphocytic leukemia (ALL) has a poor prognosis. MicroRNAs (miRNA) are small noncoding RNAs that posttranscriptionally regulate expression of target mRNAs. Our analysis of previously published data showed that expression of miR-128b and miR-221 is down-regulated in MLL-rearranged ALL relative to other types of ALL. Reexpression of these miRNAs cooperatively sensitizes 2 cultured lines of MLL-AF4 ALL cells to glucocorticoids. Target genes down-regulated by miR-128b include MLL, AF4, and both MLL-AF4 and AF4-MLL fusion genes; miR-221 down-regulates CDKN1B. These results demonstrate that down-regulation of miR-128b and miR-221 is implicated in glucocorticoid resistance and that restoration of their levels is a potentially promising therapeutic in MLL-AF4 ALL.


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