Chunk #5 — Introduction — MiR-15/16 and DLEU7 at 13q14: a unique collaboration of coding and noncoding genes in indolent CLL — MiR-15/16 at 13q14, discovery and function
BCL2 at a posttranscriptional level [15]. Consequently, BCL2 repression by these microRNAs induces apoptosis in a leukemic cell line [15], and miR-15/16 showed a tumor suppressor function in vivo by inhibiting the growth of tumor engraftments of leukemic cells in nude mice [16]. These findings suggested that deletions of miR-15/16 result in Bcl2 up-regulation, contributing to the pathogenesis of CLL. The importance of miR-15/16 was recently confirmed by a report studying CLL development in New Zealand black (NZB) mice [17]. Since these mice are susceptible to CLL, Raveche et al. carried out linkage analysis and discovered that mouse genomic region homologous to 13q14 is one of the loci associated with CLL. DNA sequencing identified a point mutation in miR-15/16 precursor and levels of miR-16 were decreased in NZB lymphoid tissues [17].
