B-cell acute lymphoblastic leukemia (B-ALL) is often associated with chromosomal 
translocations leading to the deregulation of proto-oncogenes. MicroRNAs can 
also be affected by chromosomal alterations and thus contribute to 
carcinogenesis. The microRNA, miR-125b-1, is overexpressed in B-ALL cases with 
the t(11;14)(q24;q32) translocation; therefore, we sought to determine the role 
of this microRNA in B-cell fate. We used murine pre-BI cells alongside murine 
and human leukemic B-cell lines to show that miR-125b expression enhances 
proliferation by targeting B-cell regulator of immunoglobulin heavy-chain 
transcription (Bright)/ARID3a, an activator of immunoglobulin heavy-chain 
transcription. Accordingly, this target gene was downregulated in B-ALL patients 
with the t(11;14)(q24;q32) translocation. Repression of Bright/ARID3a blocked 
differentiation and conferred a survival advantage to Ba/F3 cells under 
interleukin-3 starvation. In addition, overexpression of miR-125b protected 
pre-BI and leukemic B-cell lines from apoptosis by blockade of caspase 
activation by a mechanism that was independent of p53 and BAK1. In summary, 
miR-125b can act as an oncogene in B-ALL by targeting ARID3a and mediating its 
repression, thus leading to a blockage in differentiation, increased 
proliferation and inhibition of apoptosis.