Functional Characterization Of MiRNA In Cancer Development

Liver and breast cancers are among the leading deadly types of cancer. Altered expression of microRNAs (miRNA), an abundant class of about 22nt noncoding RNAs that mostly function as negative regulators of gene expression by directly degrading messenger RNA (mRNA) or repressing protein translation, is common in Liver and breast cancer. In this study, we demonstrate that miRNA is closely involved in the progression of Liver and breast cancers.Meastasis is the leading cause of death in patients with hepatocellular carcinoma (HCC) and microRNAs have been implicated to influence this process. Emerging evidence indicates that miR-198 is down-regulated in HCC compared to normal liver parenchyma, but the functional roles of miR-198 in HCC cells remains unexplored. Herein, we show that miR-198 directly targets c-MET via its 3'UTR. Forced expression of miR-198 decreased c-MET expression at both mRNA and protein levels and consequently diminished HGF induced phosphorylation of p44/42 MAPK in HCC cells. Forced expression of miR-198 inhibited HGF promotion of HCC cell migration and invasion in a c-MET dependent manner. In conclusion, we have identified miR-198 as a novel suppressor of HCC cell invasion by negative regulation of the HGF/c-MET pathway.The steroid hormone estrogen is closely involved in the development and progression of women breast cancer through its effects on cellular processed including cell survival and proliferation, and that is acting via the estrogen receptors. Here, we analyze the regulation of miR-26 expression in response to estrogen, by using miRNA TaqMan real-time reverse transcription-PCR experiments, we show that the expression of miR-26a and miR-26b decreases following estrogen treatment in an ER-dependent manner. We further show that enforced expression of miR-26 reduces estrogen-dependent cell growth, which was associated with suppressing the expression of GREB1. we show that miR-26 directly targets GREB1 via its 3'UTR. Forced expression of miR-26 decreased GREB1protein expression. Overall, our data indicate that the alteration of miR-26 expression in response to estrogen play a key role in estrogen-dependent cell growth and indicate the role of miR-26 in the understanding of anti-estrogen resistance of breast cancer.