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Induction of microRNA expression and processing via ERK/MAPK signaling during monocytic differentiation

ABSTRACT: This study produced a microarray-based screening for miRNAs responding to tetradecanoyl phorbol acetate (TPA) (for monocytic differentiation) treatment in various leukemia cell lines.

ORGANISM(S): Rattus norvegicus Mus musculus Homo sapiens

PROVIDER: GSE33537 | GEO | 2013/12/01

SECONDARY ACCESSION(S): PRJNA148899

REPOSITORIES: GEO

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Induction of microRNA expression and processing via ERK/MAPK signaling during monocytic differentiation

Project description:This study produced a microarray-based screening for miRNAs responding to tetradecanoyl phorbol acetate (TPA) (for monocytic differentiation) treatment in various leukemia cell lines. Using the microarray technique, global changes in miRNA expression after treatment of four leukemia cell lines (NB4, HL-60, U937 and K562) with TPA was profiled. This microarray chip contained 924 probes for 802 miRNAs from human, mouse and rat after discarding redundant sequences, and a further 122 predicted miRNA sequences from published data. To reduce individual variability, replicate array analysis used independently treated samples, and a technical replicate was also performed with the same sample.

2013-12-01 | E-GEOD-33537 | biostudies-arrayexpress

RNA-seq analysis of PMA treament with or without LPS on human monocytic cell line THP1

Project description:Transcriptome analysis of the human monocytic cell line THP1 (ATCC TIB-202) treated or not with phorbol myristate acetate (PMA) +/- lipopolysaccharides-lipopolysaccharides binding protein (LPS-LBP)

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Expression Profiles of HepG2 cells treated with following compounds: Azathriopine, Furan, Tetradecanoyl phorbol acetate, Tetrachloroethylene, Diazinon and Dmannitol

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MitomiR profiling of mitochondria extracted from monocytic cell line

Project description:MiRNAs play pivotal roles in regulating macrophage functions, including differentiation, polarization, recruitment, and activation of inflammation. in this review, to provide novel insight into macrophage differentiation-specific mitomiR signatures and associated mitochondrial pathways, we performed a global miRNA profiling on extracted mitochondria and total cell content of human macrophages. The THP-1 monocytic cell line was treated with phorbol-12-myristate-13-acetate (PMA) to induce differentiation into macrophages The human monocytic cell line THP-1 cells were differentiated into THP-1 derived macrophages with 40 ng/mL phorbol 12-myristate 13-acetate (PMA),The mitochondrial fraction of the cells were enriched and purified using anti-TOM22 microbeads (Miltenyi Biotec). After total RNA extraction, and using Taqman low-density arrays (TLDA), we performed the global miRNA profiling on extracted mitochondria and compared with total cell content

2021-12-02 | GSE182255 | GEO

U937 cells: differentiating vs. undifferentiated

Project description:Gene-expression changes in U937 cells undergoing monocytic differentiation with TPA treatment Keywords: differentiation treatment The promonocytic U937 cell line was maintained at 37C in RPMI 1640 medium (Mediatech) supplemented with 10% fetalclone (HyClone) under a 5% CO2, 95% air atmosphere. U937 cells were differentiated by the addition to the growth medium 100 nM 12-O-tetradeconoyl-phorbol 13-acetate (TPA) (Sigma).Three condition experiment, treated with TPA for two different time points (27 and 96 hrs) vs. untreated. Biological replicates: independently grown, treated and harvested

2010-06-20 | E-GEOD-10560 | biostudies-arrayexpress

Expression Profiles of HepG2 cells treated with following compounds: Azathriopine, Furan, Tetradecanoyl phorbol acetate, Tetrachloroethylene, Diazinon and Dmannitol

Project description:The transcriptomic changes induced in the human liver cell line HepG2 by Azathriopine (250M-BM-5M, Sigma-Aldrich), Furan (2mM, Sigma-Aldrich), Tetradecanoyl phorbol acetate (500nM, Sigma-Aldrich), Tetrachloroethylene (2mM, Sigma-Aldrich), Diazinon (250M-BM-5M, Sigma-Aldrich) and Dmannitol (250M-BM-5M, Sigma-Aldrich) during 4, 8, 24, 48 and 72hrs As a solvent control for Azathriopine, Furan, Diazinon and Tetradecanoyl phorbol acetate, DMSO was used (0.5%); As a solvent control for tetrachloroethylene, ethanol was used (0.5%); As a solvent control for D-mannitol, HBSS was used (0.5%) The study investigated differential gene expression in HepG2 cell line mRNA following 4, 8, 24, 48 and 72h hours of exposure to Azathriopine, Furan, Tetradecanoyl phorbol acetate, Tetrachloroethylene, Diazinon, D-mannitol, DMSO solvent control, ethanol solvent control and HBSS solvent control. Three biological replicates per compound/solvent. In total 135 arrays were analyzed in total.

2015-01-13 | E-GEOD-58235 | biostudies-arrayexpress

Reversible and irreversible anchorage independent growth in skin cells

Project description:We have investigated the regulation of anchorage-independent growth (AIG) by basic fibroblast growth factor (bFGF) and 12-O-tetradecanoyl phorbol-13-acetate (TPA) in JB6 mouse epidermal cells in the context of wound repair versus carcinogenesis responses. bFGF induces an unusually efficient but reversible AIG response, relative to TPA-induced AIG which is irreversible. Distinct global gene expression profiles are associated with anchorage-independent colonies arising from bFGF-stimulated JB6 cells, relative to colonies arising from fully tumorigenic JB6 cells (RT101), including genes exhibiting reciprocal regulation patterns. Thus, while TPA exposure results in commitment to an irreversible and tumorigenic AIG phenotype, the AIG response to bFGF is reversible with essentially complete restoration of normal cell cycle check point control following removal of bFGF from growth medium. These results are consistent with the physiological role of bFGF in promoting wound healing, and suggest that natural mechanisms exist to reverse transformative cellular phenotypes associated with carcinogenesis. Keywords: cell phenotype comparison

2009-06-01 | GSE13979 | GEO

Definition of the Ras/ERK signal induced chromatin modification at target gene promoters

Project description:Specific spectra of chromatin modifications are associated with different transcriptional states and gene regulatory elements, but relatively little is known about how such chromatin modifications are established. In particular the relationship of chromatin modifications to the activity of specific transcription factors and the signalling pathways that control them remain largely unclear. We investigated the relationship between chromatin modifications and transcription in response to Ras/ERK activationby stimulating cells with TPA (12-O-tetradecanoyl phorbol-13-acetate) for 30 minutes. Oncogenic active Ras is known to mediate the cellular response to multiple growth factors leading to the activation of immediate-early genes (IE). A key player in IE gene response is the SRF transcriptional network that we identified being crucial to mediate allegedly the entire transcriptional response downstream of Ras/ERK. The Serum response factor (SRF) is a transcription factor with low intrinsic transcriptional activity and requires the recruitment of one of two families of co-activators: the MRTFs (myocardin-related transcription factors) and the TCFs (ternary complex factors). In particular the TCF, member of the wide family of ETS transcription factors, are specifically activated by MAPK signalling downstream of Ras. Cells lacking all three TCFs are defective in responding to Ras/MAPK signalling. We analysed changes in 5 main histone modifications (H3K9acS10ph, H4K16ac, H3K27ac, H3K9acK14ac and H3K4me3) associated with active transcription by ChIP-seq in Mouse Embryonic Fibroblasts (MEFs) derived from wild type mice (MEF WT) or animals lacking all three TCFs (TCF KO). In addition the distribution of the 5 modifications have been assessed in TCF KO cells reconstituted with Elk-1 (one of the member of the TCF factos) variants.

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Transcription profiling of mouse bFGF-treated JB6 cells and fully tumorigenic JB6 cells from the RT101 cell line - reversible and irreversible anchorage independent growth in skin cells

2009-06-08 | E-GEOD-13979 | biostudies-arrayexpress

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