A strict balance between cell growth, differentiation and apoptosis is necessary for normal tissue development. Many genes are involved to make sure that developmental processes succeed in a normal spatial and temporal fashion. Genes involved in these processes require appropriate transcriptional and post-transcriptional regulation. Up to 30% of all human protein-coding genes is thought to be post-transcriptionally regulated by small RNAs, called microRNAs (miRs).1 These molecules are important in many physiological processes, including proliferation, differentiation, apoptosis and the maintenance of cell and tissue identity.2,3 If miRs or their regulatory factors do not work appropriately and disturb the above mentioned physiological processes, they may contribute to human pathologies, such as cancer. 4,5 Indeed, recent research indicates that miRs are involved in various types of cancer, including breast cancer. Experiments in cell cultures and mouse models have revealed deregulated miRs that exert either tumor suppressive or oncogenic roles in cancer cells, depending on the cellular context and on the target genes they regulate.108,145 Altered miR expression has been linked to tumor initiation, progression and metastasis.303,306 However, the exact molecular mechanism of miRs and their role in tumorigenesis still needs to be elucidated. Based on computational algorithms, many miR target genes were predicted, but relatively few miR-target interactions have been experimentally validated. Modulating miR expression in vitro or in vivo may provide a powerful tool to investigate the molecular mechanisms and target genes regulated by these small RNAs. Such studies may provide exciting steps towards the potential usefulness of miRs in improving cancer diagnosis and therapy. In this paper, the working mechanism of miRs and their involvement in human breast cancer will be discussed
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