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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling by array of prostate cancer cell line PC-3 ectopically expressing miR-34c to identify genes regulated by this microRNA

ABSTRACT: In this study we set out to characterize the mechanisms by which miR-34c deregulation contribute to PCa progression. The genes regulated by miR-34c in the prostate cancer cell line PC3 were identified by microarray analyses, and the top biofunctional pathways enriched for identified genes were found to be cell death, cell cycle, cellular growth, and cellular movement. One of the identified targets was MET, a receptor protein tyrosine kinase activated by hepatocyte growth factor, that is crucial for metastatic progression. see above A total of 6 samples. Where 3 are ectopic expression of miR-205 and 3 are ectopic expression of a scramble mimic.

ORGANISM(S): Homo sapiens

SUBMITTER: Yvonne Ceder

PROVIDER: E-GEOD-41322 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The tumour suppressor miR-34c targets MET in prostate cancer cells.

Hagman Z Z Haflidadottir B S BS Ansari M M Persson M M Bjartell A A Edsjö A A Ceder Y Y

British journal of cancer 20130806 5

<h4>Background</h4>The microRNA, miR-34c, is a well-established regulator of tumour suppression. It is downregulated in most forms of cancers and inhibits malignant growth by repressing genes involved in processes such as proliferation, anti-apoptosis, stemness, and migration. We have previously reported downregulation and tumour suppressive properties for miR-34c in prostate cancer (PCa).<h4>Methods</h4>In this study, we set out to further characterize the mechanisms by which miR-34c deregulati ...[more]

PMID: 23922103

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Identification of miR-34c targets

Project description:In this study we set out to characterize the mechanisms by which miR-34c deregulation contribute to PCa progression. The genes regulated by miR-34c in the prostate cancer cell line PC3 were identified by microarray analyses, and the top biofunctional pathways enriched for identified genes were found to be cell death, cell cycle, cellular growth, and cellular movement. One of the identified targets was MET, a receptor protein tyrosine kinase activated by hepatocyte growth factor, that is crucial for metastatic progression. see above

2013-12-01 | GSE41322 | GEO

A global transcriptome analysis of human epidermal keratinocytes upon overexpression of microRNA-34a or microRNA-34c

Project description:miR-34a and miR-34c were found up-regulated at wound-edges of human venous ulcer compared to nomal wound and the intact skin; however their biological role in keratinocytes during wound repair has not been studied. To study the genes regulated by miR-34a and miR-34c, we transfected miR-34a and miR-34c mimic into human primary epidermal keratinocytes to overexpress them. We performed a global transcriptome analysis of keratinocytes upon overexpression of miR-34a or miR-34c using Affymetrix arrays.

2019-09-04 | GSE117506 | GEO

Gene expression changes initiated by miR-34c in Dicer/Pten double knockout mouse serous epithelial cancer

Project description:miR-34c inhibits Dicer/Pten double knockout mouse serous epithelial cancer cell proliferation by inducing cell cycle arrest and apoptosis. We found that miR-34c had a more dramatic effect on inhibiting tumor cell viability than let-7b. The action of miR-34c induced tumor cell cycle arrest in G1 phase and apoptosis and was accompanied with the regulation of key genes involved in cell proliferation and cell cycle G1/S transition. miR-34c suppressed the expression of EZH2 and MYBL2, which may transcriptionally and functionally activate CDKN1C.

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Gene expression changes initiated by miR-34c in Dicer/Pten double knockout mouse serous epithelial cancer

2014-10-03 | E-GEOD-57493 | biostudies-arrayexpress

Deep sequencing of human naive CD4 T cells identifies miR-34c-5p as a novel regulator of T cell activation and HIV replication

Project description:We generated a model for miR-34c-5p overexpression by transfecting Jurkat T cell line with a pcDNA3 vector containing the pre-miR-34c-5p precursor sequence and selecting for antibiotic resistance to isolate both pools and clones of stably transfected cells (J34c cells), in parallel with control cells transfected with the empty parental vector (JÃ cells). Both pools of stably transfected cells and the derived clonal lines expressed high levels of the miR.

2016-12-21 | E-MTAB-4190 | biostudies-arrayexpress

Deep sequencing of human naive CD4 T cells identifies miR-34c-5p as a novel regulator of T cell activation and HIV replication

Project description:Cell activation is a vital step for T cell memory/effector differentiation as well as for productive HIV infection. To identify novel regulators of this process, we used next generation sequencing to profile changes in microRNA expression occurring in purified human naive CD4 T cells in response to TCR stimulation and HIV infection. HIV infection had no significant impact on global miR expression in quiescent nave CD4 T cells. We identified miR-34c-5p as a novel miR strongly induced by TCR stimulation of nave CD4 T cells, and found that it was consistently down-regulated in response to viral infection. Over-expression of miR-34c-5p had a positive effect on HIV-1 replication. Finally, we demonstrated that miR-34c-5p alters the expression of several genes involved in TCR signaling and cell activation, identifying it as a novel regulator of nave CD4 T cell activation potentially targeted by HIV infection.

2016-12-21 | E-MTAB-4214 | biostudies-arrayexpress

NGS-based miRNome reveals regulation in the miR-34/miR-449 cluster targetome in sinonasal cancers [miRNA-seq]

Project description:Using NGS-based miRNome, followed by AGO2-RIP-seq, the miR-34c and miR-449a and their direct targets were identified as factors involved in the development and progression of sinonasal cancers (SNCs). Both miR-34c and miR-449a were independent prognostic biomarkers and were associated with patient outcome.

2023-12-28 | GSE192595 | GEO

NGS-based miRNome reveals regulation in the miR-34/miR-449 cluster targetome in sinonasal cancers [RIP-seq]

2023-12-28 | GSE192594 | GEO

Molecular Mechanisms Associated with Primary Open-angle Glaucoma with MicroRNA Microarray Data

Project description:This study aimed to investigate the molecular mechanism responsible for primary open-angle glaucoma (POAG) progression. We analyzed microRNAs (miRNAs) expression profiling in aqueous humor (AH) of both POAG patients and normal controls, using a microarray-based approach. Subsequently, differentially expressed miRNAs (DEmiRNAs) were identified using Bayes moderated t-test. Next, DEmiRNAs target genes were predicted based on miRNA databases, followed by GO analysis and pathway analysis using DAVID. Furthermore, OAG-related genes analysis for target genes was carried out using CTD database, respectively. Finally, verification of DEmiRNAs expression levels was performed by RT-qPCR. A total of 40 significant DEmiRNAs were identified between control and POAG groups, including 24 up-regulated miRNAs and 16 down-regulated miRNAs. Further, the target genes of hsa-miR-206, including BMP2, SMAD4, ID2, and TNF, were mainly enriched in transforming growth factor-β (TGF-β) signaling pathway. While, target genes of hsa-miR-184, hsa-miR-34c-5p, hsa-miR-7-2-3p and hsa-miR-20b-3p, including BCL2, EPHB2, VEGFA, COL4A1, APC, and TGFBR1, were enriched in eye development. Moreover, FNDC3B, CAV2 and VEGF, target genes of hsa-miR-206 or hsa-miR-34c-5p, were the OAG-related genes. Ultimately, RT-qPCR analysis confirmed that mRNA levels of hsa-miR-206, hsa-miR-7-2-3p, and hsa-miR-20b-3p were increased, while those of hsa-miR-184 and hsa-miR-34c-5p were decreased in POAG compared with normal groups (P < 0.05). Hsa-miR-206, hsa-miR-184, hsa-miR-34c-5p, hsa-miR-7-2-3p and hsa-miR-20b-3p might play a significant role in the pathogenesis of POAG and hsa-miR-206 might be associated with the development of POAG by regulating TGF-β signaling pathway. These results might provide insight toward a better understanding of the pathogenesis of POAG.

2015-08-04 | GSE71639 | GEO

miR-625-3p regulates oxaliplatin resistance by targeting MAP2K6-p38 signaling in human colorectal adenocarcinoma cells

Project description:Oxaliplatin (oxPt) resistance in colorectal cancers (CRC) is a major unsolved problem. Consequently, predictive markers and a better understanding of resistance mechanisms are urgently needed. To investigate if the recently identified predictive miR-625-3p is functionally involved in oxPt resistance, stable and inducible models of miR-625-3p dysregulation were analyzed. Ectopic expression of miR-625-3p in CRC cells led to increased resistance towards oxPt. The mitogen-activated protein kinase (MAPK) kinase 6 (MAP2K6/MKK6) – an activator of p38 MAPK - was identified as a functional target of miR-625-3p, and, in agreement, was down-regulated in patients not responding to oxPt therapy. The miR-625-3p resistance phenotype could be reversed by anti-miR-625-3p treatment and by ectopic expression of a miR-625-3p insensitive MAP2K6 variant. Transcriptome, proteome and phosphoproteome profiles revealed inactivation of MAP2K6-p38 signaling as a possible driving force behind oxPt resistance. We conclude that miR-625-3p induces oxPt resistance by abrogating MAP2K6-p38 regulated apoptosis and cell cycle control networks.

2017-03-29 | MSV000080762 | MassIVE

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