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[Cancer Research 65, 6029-6033, July 15, 2005]
© 2005 American Association for Cancer Research

Priority Reports

MicroRNA-21 Is an Antiapoptotic Factor in Human Glioblastoma Cells

Jennifer A. Chan1,3, Anna M. Krichevsky2 and Kenneth S. Kosik4

Departments of 1 Pathology and 2 Neurology, Brigham and Women's Hospital and 3 Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts; and 4 Neuroscience Research Institute, University of California Santa Barbara, Santa Barbara, California

Requests for reprints: Anna M. Krichevsky, Neurology, Brigham and Women's Hospital, Harvard Medical School, 4 Blackfan Circle HIM 760, Boston, MA 02115. Phone: 617-525-5195; Fax: 617-525-5305; E-mail: krichevsky{at}cnd.bwh.harvard.edu.

MicroRNAs (miRNAs) are small noncoding RNA molecules that regulate protein expression by targeting the mRNA of protein-coding genes for either cleavage or repression of translation. The roles of miRNAs in lineage determination and proliferation as well as the location of several miRNA genes at sites of translocation breakpoints or deletions has led to the speculation that miRNAs could be important factors in the development or maintenance of the neoplastic state. Here we show that the highly malignant human brain tumor, glioblastoma, strongly overexpresses a specific miRNA, miR-21. Our studies show markedly elevated miR-21 levels in human glioblastoma tumor tissues, early-passage glioblastoma cultures, and in six established glioblastoma cell lines (A172, U87, U373, LN229, LN428, and LN308) compared with nonneoplastic fetal and adult brain tissues and compared with cultured nonneoplastic glial cells. Knockdown of miR-21 in cultured glioblastoma cells triggers activation of caspases and leads to increased apoptotic cell death. Our data suggest that aberrantly expressed miR-21 may contribute to the malignant phenotype by blocking expression of critical apoptosis-related genes.




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