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Regulation of gene expression by mir-493

ABSTRACT: To identify genes that are inhibited by mir-493, we have employed whole genome microarray expression profiling as a discovery platform to identify genes that are down-regulated after expression of mir-493. HCT116 colon cancer cells were transfected with control or mir-493 mimic for 24 hrs, and total RNA extracted from the transfected cells were labeled with Cy3 and used for microarray analyses with Agilent Whole Human Genome Oligo Microarrays.

ORGANISM(S): Homo sapiens

PROVIDER: GSE31751 | GEO | 2012/04/01

SECONDARY ACCESSION(S): PRJNA145329

REPOSITORIES: GEO

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Regulation of gene expression by mir-493

Project description:To identify genes that are inhibited by mir-493, we have employed whole genome microarray expression profiling as a discovery platform to identify genes that are down-regulated after expression of mir-493. HCT116 colon cancer cells were transfected with control or mir-493 mimic for 24 hrs, and total RNA extracted from the transfected cells were labeled with Cy3 and used for microarray analyses with Agilent Whole Human Genome Oligo Microarrays. gene expression in HCT116 cells was measured after transfection of control or mir-493. Three independent experiments were performed for each transfection.

2012-03-31 | E-GEOD-31751 | biostudies-arrayexpress

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Project description:Primary hepatic tumors mainly include hepatocellular carcinoma (HCC), which is one of the most frequent causes of cancer-related deaths worldwide. Thus far, HCC prognosis has remained extremely poor given the lack of effective treatments. Numerous studies have described the roles played by microRNAs (miRNAs) in cancer progression and the potential of these small noncoding RNAs for diagnostic or therapeutic applications. The current consensus supports the idea that direct repression of a wide range of oncogenes by a single key miRNA may critically affect the malignant properties of cancer cells in a synergistic manner. In this study, we aimed to investigate the oncogenes controlled by miR-493-5p, a major tumor suppressor miRNA that inactivates miR-483-3p oncomir in hepatic cancer cells. Using global gene expression analysis, we highlighted a set of candidate genes potentially regulated by miR-493-5p. In particular, the canonical MYCN proto-oncogene (MYCN) appeared to be an attractive target of miR-493-5p given its significant inhibition via 3’-UTR targeting in miR-493-5p-rescued HCC cells. We showed that MYCN was overexpressed in liver cancer cell lines and clinical samples from HCC patients. Notably, MYCN expression levels were inversely correlated with miR-493-5p in tumor tissues. We confirmed that MYCN knockdown mimicked the anti-cancer effect of miR-493-5p by inhibiting HCC cell growth and invasion, whereas MYCN rescue hindered miR-493-5p activity. In summary, miR-493-5p is a pivotal miRNA that modulates various oncogenes after its re-expression in liver cancer cells, suggesting that tumor suppressor miRNAs with a large spectrum of action may provide valuable tools for miRNA replacement therapies.

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Expression profile of HCT116 cells transfected with miR-204-5p

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Characterization of microRNA-493-5p targets in liver cell lines

Project description:Numerous studies have described the critical role played by microRNAs (miRNAs) in cancer progression and the potential of these small non-coding RNAs for diagnostic or therapeutic applications. However, the mechanisms responsible for the altered expression of miRNAs in malignant cells remain poorly understood. Herein, via epigenetic unmasking, we identified a group of miRNAs located in the imprinted delta like non-canonical Notch ligand 1 (DLK1)-maternally expressed 3 (MEG3) locus that were repressed in hepatic tumor cells. Notably, miR-493-5p epigenetic silencing was correlated with hypermethylation of the MEG3-differentially regulated region (DMR) in liver cancer cell lines and tumor tissues from patients. Experimental rescue of miR-493-5p promoted an anti-cancer response by hindering hepatocellular carcinoma (HCC) cell growth in vitro and tumor progression in vivo. We found that miR-493-5p mediated part of its tumor-suppressor activity by abrogating overexpression of insulin-like growth factor 2 (IGF2) and the IGF2-derived intronic oncomir miR-483-3p in HCC cells characterized by IGF2 loss of imprinting (LOI). In summary, this study describes an unknown miRNA-dependent regulatory mechanism between two distinct imprinted loci and a possible therapeutic window for liver cancer patients exhibiting IGF2-miR-483 LOI and amplification.

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