Journal
MOLECULAR CANCER RESEARCH
Volume 13, Issue 5, Pages 839-851Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1541-7786.MCR-15-0006-T
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Funding
- NIH [K08CA133521]
- Sidney Kimmel Foundation [SKF-11-013]
- Irving Feintech Family Foundation/Tower Cancer Research Foundation Research Grant
- University of California Cancer Research Coordinating Committee
- Stein-Oppenheimer Endowment Award, Tumor Biology Training grant from the NIH [NIH T32CA009056]
- Eugene V. Cota-Robles Fellowship from UCLA
- National Science Foundation
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Long noncoding RNAs (lncRNA) have been found to play a role in gene regulation with dysregulated expression in various cancers. The precise role that lncRNA expression plays in the pathogenesis of B-acute lymphoblastic leukemia (B-ALL) is unknown. Therefore, unbiased microarray profiling was performed on human B-ALL specimens, and it was determined that lncRNA expression correlates with cytogenetic abnormalities, which was confirmed by qRT-PCR in a large set of B-ALL cases. Importantly, high expression of BALR-2 correlated with poor overall survival and diminished response to prednisone treatment. In line with a function for this lncRNA in regulating cell survival, BALR-2 knockdown led to reduced proliferation, increased apoptosis, and increased sensitivity to prednisolone treatment. Conversely, overexpression of BALR-2 led to increased cell growth and resistance to prednisone treatment. Interestingly, BALR-2 expression was repressed by prednisolone treatment and its knockdown led to upregulation of the glucocorticoid response pathway in both human and mouse B cells. Together, these findings indicate that BALR-2 plays a functional role in the pathogenesis and/or clinical responsiveness of B-ALL, and that altering the levels of particular lncRNAs may provide a future direction for therapeutic development. (C)2015 AACR.
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