EN
MicroRNAs (miRNAs) are endogenous single-stranded non-coding RNAs of about - 22 nucleotides which suppress gene expression by selectively binding to the 3’ non coding region (3’-UTR) of specific messenger RNAs through base-pairing. There are now more than 1600 human miRNAs annotated in the miRNA registry (http://microrna.sanger.ac.uk), but, at the moment, very few miRNAs have been well characterized and most of their roles remain unknown. miRNAs derive from transcripts that fold back on themselves to form distinctive hairpin structures, whereas the other types of endogenous small RNAs derive either from much longer hairpins that give rise to a greater diversity of small RNAs (siRNAs), or from bimolecular RNA duplexes (siRNAs), or from precursors without any suspected doublestranded character (piRNAs). The key step to understanding more about the possible functions of microRNA is to identify their mRNA targets. Recent studies have supported a role of miRNAs in the initiation and progression of human malignancies. Several groups have studied the global miRNA expression in cancer patients and found that miRNAs show different patterns of expression in normal and tumor tissues. The involvement of miRNAs in human cancer is probably due to the fact that >50% of miRNA genes are located at chromosomal regions, such as fragile sites or common break point sites, and regions of deletion or amplification that are generally altered in human tumors. Experimental evidence has shown that miRNA expression profiles enable the classification of poorly characterized human tumors that cannot be accurately classified using only the mRNA expression patterns. As a result, the miRs involved in the oncogenic transformation process are being investigated as novel biomarkers of disease detection and prognosis as well as potential therapeutic targets for human cancers. The aim of this review is to provide a general background regarding current knowledge about miRNA involvement in human pancreatic cancer and in the regulation of glucose metabolism.