MicroRNAs consist selleckchem of short RNA molecules 21 base pairs in length that do not withhold the sequential information to transcribe for proteins, but instead control the transcriptional levels of a subset of target genes. It was first demonstrated in plants that miRNAs can suppress transcription of a target messenger RNA (mRNA) by base pairing with the 3′-untranslated region (UTR) of their target mRNAs.1, 2 In case of perfect or nearly perfect

pairing, the target mRNA becomes degraded. In many cases, pairing with the respective mRNAs is imperfect, leading to translational repression of the latter.3 Since their discovery, more than 1000 miRNAs have been identified in the human genome, and growing evidence points toward an important role

of many miRNAs in tumorigenesis. In the liver, different approaches were previously taken to identify miRNAs that regulate hepatocarcinogenesis. As such, miRNA expression patterns in human hepatocellular carcinoma (HCC) collectives were analyzed by the application of microarray technology.4-6 However, given the large interstudy variance of deregulated miRNAs in these studies and the frequently growing number of miRNAs that have been discovered, new intelligent screening methods are needed to find miRNAs with a functional relevance for the specific disease model of interest. The group of Xianghuo find more He at the Shanghai Cancer Institute now present a novel interesting approach to identify miRNAs that play an important role in hepatocarcinogenesis.7 Their study was based on a literature

screen of chromosomal areas with frequent amplifications or deletions occurring in HCC. Within these areas of potential chromosomal breakpoints, they identified MCE 129 miRNA-coding sequences and tested their expression in human HCC samples collected from the surgical specimen archive of the Qidong Liver Cancer Institute, Jiangsu Province, China. Semiquantitative polymerase chain reaction and genomic real-time polymerase chain reaction experiments on these specific tumor samples revealed 22 miRNAs with genome copy gains or losses. Of these, microRNA-151 (miR-151) was the most frequently amplified (56.1% gain) and showed a markedly up-regulated expression. This miRNA was shown to be localized to chromosome 8q24.3, a common recurrent amplification region in HCC.8 Moreover, it resides within intron-22 of the host gene FAK (focal adhesion kinase). The encoded protein of which is also known as PTK2 (protein thyrosine kinase 2), a key signaling molecule involved in the regulation of cell motility9 (Fig. 1), suggesting a functional synergism between the respective miRNA and its hosting gene. Indeed, expression of miR-151 showed tight correlation with FAK expression in HCC tissues and cell cultures.7 In further experiments, the authors demonstrated a functional role of miR-151 in tumor invasion and metastasis in vitro and in vivo.