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MiR-191 regulates human cell proliferation and directly targets multiple oncogenes [seq]

ABSTRACT: We constructed a genome wide target profile of hsa-miR-191 by sequencing RNA isolated from Ago2 immunoprecipitations and total RNA samples following miR-191 transfection

ORGANISM(S): Homo sapiens

PROVIDER: GSE63555 | GEO | 2015/03/01

SECONDARY ACCESSION(S): PRJNA268198

REPOSITORIES: GEO

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Gene expression after treatment with anti-miR-191 or control

Project description:The goal of this experiment was to identify possible genes affected directly or indirectly by anti-miR-191. Hepatocellular carcinoma (HCC) is a fatal disease with currently very limited beneficial therapies. MicroRNAs (miRs), which are considered to be master regulators of gene expression, have significant influence on cellular pathways and phenotype, and are de-regulated in HCC, and hence are thought to be of great therapeutic potential as novel targets. We identified hsa-miR-191 as a potential target for HCC therapy. Inhibition of this miR causes decreased cell proliferation and induction of apoptosis in vitro as well as a significant reduction of tumor mass in vivo in an orthotopic liver xenograft model. This miR was also found to be up-regulated by a dioxin, a known liver carcinogen, and was found to be a key regulator of cancer related pathways. HCC cell line treated with anti-miR-191, and treated with negative control anti-miR. Treatment was done twice (duplicates) but in independent studies.

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MiR-191 Regulates Primary Human Fibroblast Proliferation and Directly Targets Multiple Oncogenes.

Project description: Not available

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Gene expression after treatment with anti-miR-191 or control

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Project description:The goal of this experiment was to study the effectivity of miR down regulation by using an anti-miR molecule. Hepatocellular carcinoma (HCC) is a fatal disease with currently very limited beneficial therapies. MicroRNAs (miRs), which are considered to be master regulators of gene expression, have significant influence on cellular pathways and phenotype, and are de-regulated in HCC, and hence are thought to be of great therapeutic potential as novel targets. We identified hsa-miR-191 as a potential target for HCC therapy. Inhibition of this miR causes decreased cell proliferation and induction of apoptosis in vitro as well as a significant reduction of tumor mass in vivo in an orthotopic liver xenograft model. This miR was also found to be up-regulated by a dioxin, a known liver carcinogen, and was found to be a key regulator of cancer related pathways. HCC cell line treated with anti-miR-191, and treated with negative control anti-miR. Although this experiment was done with dual channel, chanels are not compared, irrelevant samples were on the reciprocal channel. Sample data tables represent relevant, single channel data.

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Expression data HEK293T cells transfected with either Ago2, Ago2 + miR-1, Ago2 + miR-124, mock

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