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Molecular and Cellular Biology, April 2008, p. 2167-2174, Vol. 28, No. 7
0270-7306/08/$08.00+0     doi:10.1128/MCB.01977-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

MicroRNAs in the miR-106b Family Regulate p21/CDKN1A and Promote Cell Cycle Progression{triangledown} ,{dagger}

Irena Ivanovska,* Alexey S. Ball, Robert L. Diaz, Jill F. Magnus, Miho Kibukawa, Janell M. Schelter, Sumire V. Kobayashi, Lee Lim, Julja Burchard, Aimee L. Jackson, Peter S. Linsley, and Michele A. Cleary

Rosetta Inpharmatics LLC, Seattle, Washington 98109

Received 1 November 2007/ Returned for modification 10 December 2007/ Accepted 7 January 2008

microRNAs in the miR-106b family are overexpressed in multiple tumor types and are correlated with the expression of genes that regulate the cell cycle. Consistent with these observations, miR-106b family gain of function promotes cell cycle progression, whereas loss of function reverses this phenotype. Microarray profiling uncovers multiple targets of the family, including the cyclin-dependent kinase inhibitor p21/CDKN1A. We show that p21 is a direct target of miR-106b and that its silencing plays a key role in miR-106b-induced cell cycle phenotypes. We also show that miR-106b overrides a doxorubicin-induced DNA damage checkpoint. Thus, miR-106b family members contribute to tumor cell proliferation in part by regulating cell cycle progression and by modulating checkpoint functions.

* Corresponding author. Mailing address: Rosetta Inpharmatics LLC, 401 Terry Ave. N, Seattle, WA 98109. Phone: (206) 802-7364. Fax: (206) 802-6388. E-mail: irena_ivanovska{at}merck.com

{triangledown} Published ahead of print on 22 January 2008.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

Molecular and Cellular Biology, April 2008, p. 2167-2174, Vol. 28, No. 7
0270-7306/08/$08.00+0     doi:10.1128/MCB.01977-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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