HMGA2 overexpression is associated with differential expression of miRNAs in uterine leiomyomas

Background Uterine leiomyomas (UL) are mesenchymal benign tumors extremely common that represent a significant public health problem. The deregulation of growth factors and microRNAs (miRNAs), shortening of telomeres, excessive production of disorganized extracellular matrix, loss of heterozygosity and recurrent chromosomal aberrations (including 7q22 deletion and chromossomal rearrangements in 12q15) have been suggested to contribute to the growth of fibroids. HMGA2, mapped to 12q15, is a major regulator of benign tumorigenesis from mesenchyme-derived tissues and stem-cell self-renewal. In UL, HMGA2 overexpression is frequently reported. Recently it has been shown that repression of HMGA2 by microRNA let-7s is a critical molecular regulatory mechanism associated with tumor growth. In this study, it was evaluated three miRNAs mapped to 7q22 (miR-25, miR-93 and miR106b) and miR-let-7a (previously reported as HMGA2 regulator). These findings were compared with gene expression microarray data.