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Expression data from human primary fibroblasts (IMR90) stably expressing H-RasV12 and treated with Metformin or vehicle

ABSTRACT: Metformin reduces the incidence of cancer in diabetics or in animal models. At the cellular level, the effects of metformin include the inhibition of complex I of the mitochondrial electron transport chain, a reduction in ATP levels and the activation of the energy sensor AMP kinase. Metformin also prevents the production of reactive oxygen species in primary human cells expressing oncogenic ras and the DNA damage associated to the process. We used microarrays to characterize the gene expression changes induced by metformin in primary human fibroblasts expressing oncogenic ras.

ORGANISM(S): Homo sapiens

PROVIDER: GSE33612 | GEO | 2013/04/01

SECONDARY ACCESSION(S): PRJNA148507

REPOSITORIES: GEO

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Expression data from human primary fibroblasts (IMR90) stably expressing H-RasV12 and shRNA against ERK2 or a non-targeting shRNA

Project description:Oncogenic ras activates several signaling pathways that cooperate in cell transformation. They include the ERK/MAP kinase pathway, the PI3K pathway and the Ral pathway among others. Surprisingly, in primary human fibroblasts, oncogenic ras expression induces senescence not transformation, but upon knockdown of ERK2 senescence is bypassed and transformation is stimulated. We used microarrays to characterize the gene expression programme of cells transformed by oncogenic ras, telomerase and knockdown of the ERK2 kinase. Primary human fibroblasts were co-infected with a retroviral vector that expresses oncogenic ras and either a control shRNA or an shRNA against ERK2. Cells with oncogenic ras and shRNA control entered senescence while cells with oncogenic ras and shRNA ERK2 bypassed senescence and underwent malignant transformation. Triplicates of these populations were used to purify total RNA, which we sent to Genome Quebec service for hybridization with Affymetrix microarrays.

2014-10-01 | E-GEOD-33613 | biostudies-arrayexpress

Expression data from human primary fibroblasts (IMR90) stably expressing H-RasV12 and shRNA against ERK2 or a non-targeting shRNA

2014-10-01 | GSE33613 | GEO

Distinct perturbation of the translatome by the anti-diabetic drug metformin

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2012-05-20 | E-GEOD-36847 | biostudies-arrayexpress

Evaluation of microRNA expression in vehicle and metformin-treated breast cancer cells and evaluation of the dicer relevance

Project description:We have evaluated the microRNA expression profile of SUM159 cells stably infected with a control shRNA or a dicer-targeting shRNA treated with vehicle or metformin for 24 hrs at non cytotoxic doses. microRNA expression was evaluated from total RNA extracted from logaritmically growing SUM159 cells stably expressing a control shRNA or a dicer-targeting shRNA and treated with vehicle (PBS) or metformin (0.5mM) for 24 hrs.

2012-06-04 | E-GEOD-37038 | biostudies-arrayexpress

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2012-05-21 | GSE36847 | GEO

Metformin Induces Dicer via Regulation of the RNA-binding protein AUF1

Project description:Metformin has been commonly used for decades to treat type 2 diabetes. Recent data indicates that mice treated with metformin live longer and healthier lives. Here, we show that chronic metformin exposure in mice and diabetics taking metformin have higher levels of the microRNA processing protein, Dicer. Examination of how metformin affects Dicer expression revealed that metformin alters binding of the AUF1 RNA-binding protein to DICER1 mRNA, which leads to stabilization of DICER1 mRNA. We found differential changes in microRNA expression in mice treated with metformin or caloric restriction, a proven life extending intervention. Several of these microRNAs are important for regulating cellular senescence and lifespan in model organisms. Consistent with this observation, treatment with metformin decreased cellular senescence in a Dicer-dependent manner. These data lead us to hypothesize that changes in Dicer levels may be important for organismal aging and that interventions that upregulate Dicer expression (e.g., metformin) may offer new therapeutic approaches to combat or prevent age-related diseases. Key words: diabetes mellitus, metformin, senescence, miRNA, RNA-binding proteins

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