406989

MIR206

MIRN206|miRNA206;microRNA 206;MIR206;microRNA 206

-

6p12.2

miscRNA

Count: 2; Pubmed_search,Generif

This study investigated the role of miR-206 in estrogen receptor-alpha (ERalpha)-positive endometrial endometrioid adenocarcinoma (EEC). We profiled miR-206 expression in 30 EEC clinical samples using qRT-PCR, and explored its relationship with ERalpha and clinical parameters. A luciferase reporter assay assessed the ERalpha targeting potential of miR-206. Functional analyses of miR-206 were performed in EEC cell lines. miRNA-206 expression decreased in ERalpha-positive EECs, and its expression was negatively correlated with ERalpha. miRNA-206 overexpression inhibited ERalpha-dependent proliferation, impaired invasiveness and induced cell cycle arrest of ERalpha-positive EEC cell lines. Therefore, aberrantly expressed miRNA-206 may be associated with the development of ERalpha-positive EEC.CI - Copyright (c) 2011 Elsevier Ireland Ltd. All rights reserved.

microRNAs (miRNAs) are a major class of small endogenous RNA molecules that post-transcriptionally inhibit gene expression. Many miRNAs have been implicated in several human cancers, including breast cancer. Here we describe the association between altered miRNA signatures and breast cancer tumorigenesis and metastasis. The loss of several tumor suppressor miRNAs (miR-206, miR-17-5p, miR-125a, miR-125b, miR-200, let-7, miR-34 and miR-31) and the overexpression of certain oncogenic miRNAs (miR-21, miR-155, miR-10b, miR-373 and miR-520c) have been observed in many breast cancers. The gene networks orchestrated by these miRNAs are still largely unknown, although key targets have been identified that may contribute to the disease phenotype. Here we report how the observed perturbations in miRNA expression profiles may lead to disruption of key pathways involved in breast cancer.

microRNAs (miRNAs) are endogenous short (approximately 22) nucleotide RNAs that regulate gene function by modification of target mRNAs. miRNA-1 (miR-1) and miRNA-206 (miR-206) are highly expressed in skeletal muscle. Due to the tissue-specific nature of miR-1/206 for skeletal muscles, we investigated the role of miR-1/206 in the development of rhabdomyosarcoma. Initially, we demonstrated that miR-1/206 expression was suppressed in rhabdomyosarcomas and found at very low levels in a rhabdomyosarcoma RD cell line. Transient transfection of miR-1/206 into cultured RD cells led to a significant decrease in cell growth and migration. Using bioinformatics, we identified two putative miR-1/206 binding sites within the 3'-untranslated region of the human c-Met mRNA. miR-1/206 was then shown to have activity on mRNA expression by targeting the c-Met 3'-untranslated region. The expression of c-Met protein was shown to be down-regulated by subsequent Western blot analysis. Conversely, up-regulation of c-Met was confirmed in tissue samples of human rhabdomyosarcoma, with its level inversely correlated with miR-1/206 expression. In vivo, miR-1/206-expressing tumor cells showed growth delay in comparison with negative control. Our results demonstrated that miR-1/206 suppressed c-Met expression in rhabdomyosarcoma and could function as a potent tumor suppressor in c-Met-overexpressing tumors. Inhibition of miR-1/206 function could contribute to aberrant cell proliferation and migration, leading to rhabdomyosarcoma development.