Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from miR-92 over-expressing R26MER/MER mouse embryonic fibroblast (MEFs)


ABSTRACT: miR-92 enhances c-Myc induced apoptosis. In the R26MER/MER mouse embryonic fibroblasts (MEFs), a switchable variant of Myc, MycERT2, was knocked into the genomic region downstream of the constitutive Rosa26 promoter, allowing acute activation of c-Myc by 4-OHT-induced nuclear translocation. This in vitro system nicely recapitulates c-Myc-induced apoptosis, as activated MycERT2 induces strong p53-dependent apoptosis in response to serum starvation. Enforced miR-92 expression in three independent R26MER/MER MEF lines significantly enhanced Myc-induced apoptosis. We used microarrays to investigate the molecular mechanism underlying miR-92 functions. Three independent R26MER/MER MEF lines were infected by MSCV vector alone or by MSCV vector encoding miR-92. These MEFs were serum starved and 4-OHT treated to trigger strong Myc-induced apoptosis.

ORGANISM(S): Mus musculus

SUBMITTER: Lin He 

PROVIDER: E-GEOD-53225 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications


mir-17-92, a potent polycistronic oncomir, encodes six mature miRNAs with complex modes of interactions. In the Eμ-myc Burkitt's lymphoma model, mir-17-92 exhibits potent oncogenic activity by repressing c-Myc-induced apoptosis, primarily through its miR-19 components. Surprisingly, mir-17-92 also encodes the miR-92 component that negatively regulates its oncogenic cooperation with c-Myc. This miR-92 effect is, at least in part, mediated by its direct repression of Fbw7, which promotes the prote  ...[more]

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