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Inactivated LRRC4 has been clinically detected in gliomas, and promoter hypermethylation has been implicated as the mechanism of inactivation in some of those tumors. Our previous researches indicated that LRRC4 is a target gene of miR-381, the interaction of miR-381 and LRRC4 is involved in glioma growth. In this study, we demonstrate that LRRC4 is a target gene of the other microRNA, miR-182. We found that the high expression of miR-182 and miR-381 in gliomas are involved in pathological malignant progression. The silencing of miR-182 and miR-381 inhibited the proliferation in vitro and growth of glioma cell with in vivo magnetic resonance imaging by intracranial transplanted tumor model in rats. We also demonstrated that BRD7, a transcriptional cofactor for p53, is highly expressed and negatively correlated with LRRC4 expression in gliomas. Disturbing miR-182 and miR-381 affected transcriptional regulation of the BRD7 gene. This finding was verified by ectopic overexpression of LRRC4 or restoration of endogenous LRRC4 expression by treatment with the DNA demethylating agent 5-Aza-dC. Taken together, miR-182 and miR-381 may be a useful therapeutic target for treatment of glioma. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) is a common malignant gastrointestinal cancer. Efforts for preventive and personalized medicine have intensified in the last decade with attention to novel forms of biomarkers. In the present study, microRNA and genetic analyses were performed in tandem for differential transcriptome profiling between primary tumors with or without nodes or distant metastases. Serial Test Cluster (STC) analysis demonstrated that 20 genes and two microRNAs showed distinctive expression patterns associated with the tumor, node, and metastasis (TNM) stage. The selected target genes were characterized by GO and Pathway analysis. A microRNA-target gene network analysis showed that miR-429 resided in the center of the network, indicating that miR-429 might serve important roles in the development of CRC. Real-time PCR and tissue microarrays showed that miR-429 had a dynamic expression pattern during the CRC progression stage, and was significantly downregulated in stage II and stage III clinical progression. The low expression of miR-429 was correlated with poor prognosis for CRC. Taken together, miR-429 warrant further clinical translation research as a candidate biomarker for CRC prognosis. Additional downstream targets and attendant gene function also need to be discerned to design a sound critical path to personalized medicine for persons susceptible to, or diagnosed with CRC. [ABSTRACT FROM AUTHOR]