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Expression data from multiple myeloma cells

ABSTRACT: Melphalan-induced modulation of miR-221/222 levels in MM cells. Melphalan-resistant U266/LR7 cells showed the highest induction of miR-221/222 after drug exposure. To study the transcriptome perturbation induced in MM cells following the combination of miR-221/222 inhibitors plus melphalan we used the whole gene expression data

ORGANISM(S): Homo sapiens

PROVIDER: GSE66618 | GEO | 2015/09/08

SECONDARY ACCESSION(S): PRJNA277463

REPOSITORIES: GEO

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Expression data from multiple myeloma cells

Project description:Melphalan-induced modulation of miR-221/222 levels in MM cells. Melphalan-resistant U266/LR7 cells showed the highest induction of miR-221/222 after drug exposure. To study the transcriptome perturbation induced in MM cells following the combination of miR-221/222 inhibitors plus melphalan we used the whole gene expression data total RNA was obtained after single or combination treatment of the Melphalan-resistant U266/LR7 cells and the parental cell line U266/s

2015-09-08 | E-GEOD-66618 | biostudies-arrayexpress

MiR-221/222 suppression induced by activation of the cAMP/PKA/CREB1 pathway is required for cAMP-induced bidirectional differentiation of glioma cells [miRNA]

Project description:Factors that increase cAMP levels can induce lineage-specific differentiation of glioma cells into astrocyte-like cells. However, the differentiation pattern and underlying mechanisms remain unclear. Here, we find that cAMP/PKA/CREB1-induced miR-221/222 suppression contributes to the neuron-like differentiation of gliomas. cAMP agonists selectively induced neuron- and astrocyte-like but not oligodendrocyte-like differentiation of C6 glioma cells. PKA inhibitors and CREB1 knockout blocked neuron-like differentiation of glioma cells. cAMP inhibited miR-221/222 in a PKA/CREB1 dependent manner. Importantly, both in vitro and in vivo assays demonstrated that transcriptional suppression of miR-221/222 is required for neuronal differentiation of glioma cells. Our findings suggest that increasing cAMP levels can induce bidirectional differentiation of glioma cells. Furthermore, the miR-221/222 cluster acts as an epigenetic brake during glioma differentiation. Factors that increase cAMP levels can induce lineage-specific differentiation of glioma cells into astrocyte-like cells. However, the differentiation pattern and underlying mechanisms remain unclear. Here, we find that cAMP/PKA/CREB1-induced miR-221/222 suppression contributes to the neuron-like differentiation of gliomas. cAMP agonists selectively induced neuron- and astrocyte-like but not oligodendrocyte-like differentiation of C6 glioma cells. PKA inhibitors and CREB1 knockout blocked neuron-like differentiation of glioma cells. cAMP inhibited miR-221/222 in a PKA/CREB1 dependent manner. Importantly, both in vitro and in vivo assays demonstrated that transcriptional suppression of miR-221/222 is required for neuronal differentiation of glioma cells. Our findings suggest that increasing cAMP levels can induce bidirectional differentiation of glioma cells. Furthermore, the miR-221/222 cluster acts as an epigenetic brake during glioma differentiation.

2021-08-24 | GSE182498 | GEO

Gene expression profiling of MCF10A (miR-221/222 vs control)

Project description:Analysis of gene expression of MCF10A to identify the targets of miR-221 and miR-222 Keywords: MCF10, miR-221, miR-222

2011-06-14 | GSE29327 | GEO

mRNA Breast Cancer Cell Line Profiles

Project description:mRNA breast cancer cell lines were profiled to study the function of hsa-mir-221 and hsa-mir-222. MCF7 cell lines were profiled after treatment with mir-221/222 mimics, and compared to profiles with transfection controls. Similarly, MDA-MB-231 cell lines were profiled after treatment with mir-221/222 inhibitors, and compared to profiles with transfection controls. Since ESR1 is a predicted target of mir-221/222 we also profiled MCF7 cell lines after disrupting ESR1 with an siRNA. Other breast cancer cell lines are provided because all cell lines were normalized together. Keywords: breast cancer, cell line, hsa-mir-221, hsa-mir-222, ESR1

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miR-221/222 drive synovial fibroblast expansion and pathogenesis of TNF-mediated arthritis

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2011-01-29 | GSE19777 | GEO

Identification of genes differentially expressed in lung cancer cells after the transfection of miR-221 or miR-222.

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2015-05-22 | E-GEOD-57676 | biostudies-arrayexpress

Transcription profiling of micro-RNA genes in human papillary thyroid carcinoma

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2007-09-01 | E-GEOD-3467 | biostudies-arrayexpress

Adipocyte Differentiation of Immortalized Human Bone Marrow-derived Stromal Cells is Modulated by microRNA-155, microRNA-221 and microRNA-222

Project description:Human bone marrow mesenchymal stromal cells are capable of limited self-renewal and multi-lineage differentiation in vitro. Several studies have demonstrated that microRNAs, post-transcriptional modifiers of protein expression, play crucial roles in the regulation of these complex processes. To gain knowledge regarding the role of microRNAs in human adipocyte regulation, we examined the microRNA expression profile of the immortalized human bone marrow-derived stromal cell line hMSC-Tert20. We identified 12 microRNAs that were differentially expressed during adipogenesis, of which several have previously been shown to play important roles in adipocyte biology. The expression of miR-155, miR-221 and miR-222 decreased during the adipogenic program, suggesting that they act as negative regulators of differentiation. Interestingly, adenovirus-mediated expression of either miR-155 alone or miR-221 plus miR-222 significantly inhibited adipogenesis and repressed induction of the master regulators C/EBP α and PPARgamma Our study provides the first experimental evidence that miR-155, miR-221 and miR-222 function in human adipocyte differentiation.

2011-08-23 | GSE24898 | GEO

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