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Differentially expressed miRNAs in TGF-β1-knock down rhabdmyosarcoma cell lines vs controls

ABSTRACT: To investigate the role of TGF-β1-regulated miRNAs in the progression of RMS,we performed comprehensive miRMA microarray analysis on RNA derived from typical RMS cell lines and TGF-β1 knock-down cell lines. We identified a novel set of TGF-β1-related miRNAs.

ORGANISM(S): Merkel cell polyomavirus Mus musculus Rattus norvegicus Human gammaherpesvirus 8 Human alphaherpesvirus 2 JC polyomavirus Betapolyomavirus macacae Murid gammaherpesvirus 4 Homo sapiens Human immunodeficiency virus 1 Human betaherpesvirus 5 Human alphaherpesvirus 1 Betapolyomavirus hominis human gammaherpesvirus 4 Mus musculus cytomegalovirus 2 Murid betaherpesvirus 1

PROVIDER: GSE40843 | GEO | 2012/09/13

SECONDARY ACCESSION(S): PRJNA175070

REPOSITORIES: GEO

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Differentially expressed miRNAs in TGF-β1-knock down human colorectal cancer cell lines vs controls

Project description:To investigate the role of TGF-β1-regulated miRNAs in the progression of colorectal cancer,we performed comprehensive miRMA microarray analysis on RNA derived from typical human colorectal cancer cell lines and TGF-β1 knock-down human colorectal cancer cell lines. We identified a novel set of TGF-β1-related miRNAs.

2013-12-16 | GSE53338 | GEO

Differentially expressed miRNAs in TGF-β1-knock down mice CT26 colorectal cancer cell lines vs controls

Project description:To investigate the role of TGF-β1-regulated miRNAs in the progression of colorectal cancer,we performed comprehensive miRMA microarray analysis on RNA derived from CT26 cell lines and TGF-β1 knock-down CT26 cell lines. We identified a novel set of TGF-β1-related miRNAs.

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Differentially expressed miRNAs in TGF-M-NM-21-knock down rhabdmyosarcoma cell lines vs controls

Project description:To investigate the role of TGF-M-NM-21-regulated miRNAs in the progression of RMS,we performed comprehensive miRMA microarray analysis on RNA derived from typical RMS cell lines and TGF-M-NM-21 knock-down cell lines. We identified a novel set of TGF-M-NM-21-related miRNAs. Total RNA was isolated from TGF-M-NM-21-knock down rhabdmyosarcoma cell lines and controls. Three-condition experiment: shRNA-TGF-M-NM-21/RD cells vs. shRNA-Control/RD cells, shRNA-TGF-M-NM-21/SMS-CTR cells vs. shRNA-Control/ SMS-CTR cells, and shRNA-TGF-M-NM-21/RH28 cells vs. shRNA-Control/RH28 cells. Biological replicates: 1 RD cells stably transfected with shRNA-TGF-M-NM-21- pSUPER gfp-neo, 1SMS-CTR cells stably transfected with shRNA-TGF-M-NM-21- pSUPER gfp-neo, 1RH28 cells stably transfected with shRNA-TGF-M-NM-21- pSUPER gfp-neo, 1RD cells stably transfected with shRNA-Control- pSUPER gfp-neo, 1SMS-CTR cells stably transfected with shRNA-Control- pSUPER gfp-neo, and 1RH28 cells stably transfected with shRNA-Control- pSUPER gfp-neo, independently grown and harvested. One replicate per array.

2012-09-13 | E-GEOD-40843 | biostudies-arrayexpress

Transcriptomic Changes in TGF-β1 Differentiated and PGE2 Dedifferentiated Myofibroblasts

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TGF-β1 alter the SARS-CoV2 pathogenesis and modulates ACE2 expression by miRNA dependent mechanism

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Differentially expressed miRNAs in TGF-M-NM-21-knock down human colorectal cancer cell lines vs controls

Project description:To investigate the role of TGF-M-NM-21-regulated miRNAs in the progression of colorectal cancer,we performed comprehensive miRMA microarray analysis on RNA derived from typical human colorectal cancer cell lines and TGF-M-NM-21 knock-down human colorectal cancer cell lines. We identified a novel set of TGF-M-NM-21-related miRNAs. Total RNA was isolated from TGF-M-NM-21-knock down colorecatl cancer cell lines and controls.Three-condition experiment: shRNA-TGF-M-NM-21/Lovo cells vs. shRNA-Control/Lovo cells, shRNA-TGF-M-NM-21/SW620 cells vs. shRNA-Control/ SW620 cells, and shRNA-TGF-M-NM-21/HT29 cells vs. shRNA-Control/HT29 cells. Biological replicates: 1 Lovo cells stably transfected with shRNA-TGF-M-NM-21- pSUPER gfp-neo, 1SW620 cells stably transfected with shRNA-TGF-M-NM-21- pSUPER gfp-neo, 1HT29 cells stably transfected with shRNA-TGF-M-NM-21- pSUPER gfp-neo, 1Love cells stably transfected with shRNA-Control- pSUPER gfp-neo, 1SW620 cells stably transfected with shRNA-Control- pSUPER gfp-neo, and 1HT29 cells stably transfected with shRNA-Control- pSUPER gfp-neo, independently grown and harvested. One replicate per array.

2013-12-16 | E-GEOD-53338 | biostudies-arrayexpress

Transcriptomic profiling of MGT#1-mVenus-reporter harboring A549 and H1944 cells upon stimulation with GSK126 and TGF-β1.

Project description:Investigation of gene expression profiles of MGT#1-mVenus-reporter harboring A549 and H1944 lung cancer cell lines upon PRC2 inhibition (GSK126) and activation of TGF-β1 pathway (TGF-β1).

2023-08-20 | GSE240898 | GEO

Genome-wide transcript profiling for native porcine valvular interstitial cells and those cultured on TCPS and treated with TGF-β1

Project description:Fibrotic diseases have significant health impact and have been associated with differentiation of the resident fibroblasts into myofibroblasts. In particular, stiffened extracellular matrix and TGF-β1 in fibrotic lesions have been shown to promote pathogenic myofibroblast activation and progression of fibrosis in various tissues. To better understand the roles of mechanical and chemical cues on myofibroblast differentiation and how they may crosstalk, we cultured primary valvular interstitial cells (VICs) isolated from porcine aortic valves and studied how traditional TCPS culture, which presents a non-physiologically stiff environment, and TGF-β1 affect native VIC phenotypes. We carried out gene expression profiling using porcine genome microarrays from Affymetrix and found that traditional TCPS culture induces major changes in gene expression of native VICs, rendering these cells more activated and similar to cells treated with TGF-β1. We also monitored time-dependent effects induced by TGF-β1 by examining gene expression changes induced by TGF-β1 at 8 hours and 24 hours. Porcine aortic VICs were isolated and cultured with or without TGF-β1 treatment for RNA extraction and hybridization on Affymetrix microarrays. We included 3 biological replicates for each condition. P0 VICs were freshly isolated cells which had not been cultured. P2 VICs were cells that had been passaged 2 times and cultured on plastic plates in low serum media. Some of the P2 VICs were treated with TGF-β1 at 5ng/ml for 8 hours or 24 hours. All the control and TGF-β1-treated conditions were collected at the same time on day 3 of culture.

2013-09-02 | E-GEOD-48839 | biostudies-arrayexpress

A novel non-canonical signaling pathway mediates TGF-β1-induced glucocorticoid insensitivity in epithelial cells

Project description:Limited therapeutic responses to glucocorticoids in chronic inflammatory disease are partly attributable to interleukins and transforming growth factor-β1 (TGF-β1). Global inhibition of TGF-β1 carries known risks, including autoimmune disease. Here we elucidate the signaling pathway subserving modulation of glucocorticoid activity by TGF-β1. The proteomic response of airway epithelial cells to TGF-β1 revealed 24 candidate proteins of which 3 were prioritized by exclusion of changes induced by: TGF-β2, which lacks the modulatory activity of TGF-β1 and TGF-β3; and those of TGF-β1 that were prevented by small molecule inhibitors of non-canonical TGF-β1 signaling, that did not prevent glucocorticoid modulation. Pharmacological and genetic approaches establish that TGF-β1-induced glucocorticoid insensitivity is mediated by a novel signaling cascade involving LIM domain kinase 2 mediated phosphorylation of phospho-cofilin1 that activates phospholipase D to generate the effector(s) (lyso)phophatidic acid. This study identifies several promising drug targets that potentially enable safe modulation of TGF-β1 in chronic inflammatory diseases.

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TGF-β1 activates neutrophil signaling and transcription but not migration

Project description:Tumor-associated neutrophils are found in many types of cancer and are often reported to contribute to negative outcomes. Several studies have shown that the presence of TGF-β in the tumor microenvironment contributes to the skewing of neutrophils to have a more pro-tumor phenotype. However, the direct effects of TGF-β on neutrophil signaling and migration are unclear. We sought to characterize TGF-β signaling in both primary human neutrophils and the neutrophil-like cell line HL-60 and determine whether TGF-β directly induces neutrophil migration. We found that TGF-β1 does not induce neutrophil migration in either a transwell or an underagarose migration assay. However, TGF-β1 does activate signals canonically through SMAD3 and noncanonically through ERK1/2 in neutrophils in a time and dose-dependent manner. Additionally, TGF-β1 present in the tumor-conditioned media (TCM) is responsible for SMAD3 activation. Moreover, we discovered that TCM from aggressive breast cancer cells induces neutrophils to secrete leukotriene B4 (LTB4), which is a lipid mediator important for amplifying neutrophil recruitment. However, we found that TGF-β1 alone does not induce secretion of LTB4. We next performed RNA-sequencing to evaluate the effects of TGF-β1 and TCM on the neutrophil transcriptome. We found that TGF-β1 and TCM result in changes in gene transcription in HL-60 cells, specifically of two pro-tumor genes OSM and VEGFA. Together, our findings characterize the effects of TGF-β1 on neutrophil signaling, migration, and gene expression that can be applied to understanding the changes in neutrophils that occur in the tumor microenvironment.

2023-08-10 | GSE230490 | GEO

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