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The posttranscriptional regulation of miRNAs is important for organism development. To investigate the role of miRNAs in angiogenesis, we performed a loss-of-function screening assay in human umbilical vein endothelial cells (HUVECs) and found that knockdown of 7 miRNAs (miR-95a, miR-126, miR-129, miR-137, miR-139, miR-200a, and miR-335) significantly suppressed cell viability. As miR-200a was highly expressed in HUVECs, blocking endogenous miR-200a using 2′-OMe antisense oligonucleotide (ASOs) resulted in a decrease of cell viability and migration. Bioinformatics analysis indicates the 3′ untranslated region (UTR) of thrombospondin-1 (THBS1) has a putative binding site for miR-200a. MiR-200a can directly bind to THBS1 3′UTR and negatively regulate THBS1 expression. The identification of endothelial cells (ECs) related miRNA and its target gene may gain new insight into the mechanism of angiogenesis. © 2011 IUBMB IUBMB Life, 63(7): 553-559, 2011 [ABSTRACT FROM AUTHOR]

MicroRNAs are small noncoding RNAs that negatively regulate target mRNAs at the posttranscription level. Here, we show that miR-16 is upregulated in human laryngeal carcinoma tissues. Inhibition of miR-16 in HEp-2 laryngeal cancer cell line could suppress cell migration and enhance cell-cell adhesion. Subsequently, zyxin, whose expression is negatively regulated by miR-16, is confirmed to be a direct target gene of miR-16. Furthermore, overexpression of zyxin could also restrain cell movement and enhance cell-cell adhesion. The study of miR-16 and its target zyxin will shed light on diagnosis and therapy of laryngeal cancer. © 2011 IUBMB IUBMB Life, 63(2): 101-108, 2011 [ABSTRACT FROM AUTHOR]

Earlier studies identified testes-specific protease 50 ( TSP50), which encodes a threonine protease, and showed that it was abnormally reactivated in many breast cancer biopsies. Further, it was shown to be negatively regulated by the p53 gene. However, little is known about the biological function of TSP50. In this study, we applied RNA interference to knockdown TSP50 gene expression in P19 murine embryonal carcinoma stem cells and tested whether this modulated the cell phenotype. The results showed that downregulation of TSP50 expression not only reduced cell proliferation, colony formation, and migration but also induced cell apoptosis. Further investigation revealed that knockdown of TSP50 resulted in greater sensitivity to doxorubicin-induced apoptosis and that activation of caspase-3 was involved in this process. © 2010 IUBMB IUBMB Life, 2010 [ABSTRACT FROM AUTHOR]

MicroRNAs are a group of endogenously expressed, single-stranded, 18–24 nt RNAs that regulate diverse cellular pathways. Although documented evidence indicates that some microRNAs can function as oncogenes or tumor-suppressors, the role of miR-214 in regulating human cervical cancer cells remains unexplored. We determined the expression level of miR-214 and found it is downregulated in cervical cancer compared with normal tissue. Overexpression of miR-214 in HeLa cells, a human cervical cancer cell line, significantly inhibited cell proliferation according to the MTT and colony forming assays. HeLa cells that stably overexpress miR-214 downregulate the expression of MEK3 and JNK1 at both mRNA and protein levels. Further investigation revealed that miR-214 regulates the expression of MEK3 and JNK1 by targeting the 3′UTRs of these genes. Collectively, these results suggest that miR-214 negatively regulates HeLa cell proliferation by targeting the noncoding regions of MEK3 and JNK1 mRNAs. © 2009 IUBMB IUBMB Life, 61(11): 1075–1082, 2009 [ABSTRACT FROM AUTHOR]