MiRNA profile in colon cancer cell culture
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Massimo Carella
PROVIDER: E-MTAB-2704 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:MicroRNA (miRNA) expression profiling identified miR-638 as one of the most significantly overexpressed miRNAs in metastatic lesions compared with primary melanomas. miR-638 enhanced the tumourigenic properties of melanoma cells in vitro and lung colonization in vivo. mRNA expression profiling of miR-638 and antagomir-transduced cells identified new candidate genes as miR-638 targets, the majority of which is involved in p53-mediated apoptosis regulation. miR-638 depletion stimulated expression of p53 and its downstream target genes and induced apoptosis and autophagy in melanoma cells. miR-638 promoter analysis revealed transcription factor associated protein 2-? (TFAP2A) as a direct negative regulator of miR-638. Further analyses provided strong evidence for a double negative regulatory feedback loop between miR-638 and TFAP2A. Taken together, miR-638 may support melanoma progression by suppressing p53-mediated apoptosis pathways and by targeting the transcriptional repressor TFAP2A. Whole genome cDNA microarray (Illumina Human HT-12 v4 Expression BeadChip Kit, San Diego, CA 92122 USA) analyses were performed in duplicates using RNA extracted from SK-Mel-147 cells transfected with a non-targeting control, miR-638 or antagomiR-638.
2014-01-30 | E-GEOD-54493 | biostudies-arrayexpress
Project description:Defects in stress responses are important contributors in many chronic conditions including cancer, cardiovascular disease, diabetes, and obesity-driven pathologies like non-alcoholic steatohepatitis (NASH). Specifically, endoplasmic reticulum (ER) stress is linked with these pathologies and control of ER stress can ameliorate tissue damage. MicroRNAs have a critical role in regulating diverse stress responses including ER stress. Here we show that miR-494-3p plays a functional role during ER stress. ER stress inducers (tunicamycin and thapsigargin) robustly increase the expression of miR-494 in vitro in an ATF6 dependent manner. Surprisingly, miR-494 pretreatment dampens the induction and magnitude of ER stress in response to tunicamycin in endothelial cells. Conversely, inhibition of miR-494 increases ER stress de novo and amplifies the effects of ER stress inducers. Using Mass Spectrometry (TMT-MS) we identified many proteins that are downregulated by both tunicamycin and miR-494 in cultured human umbilical vein endothelial cells (HUVECs). Among these, we found 6 transcripts which harbor a putative miR-494 binding site. Our data indicates that ER stress driven miR-494 may act in a feedback inhibitory loop to dampen downstream ER stress signaling. We propose that RNA-based approaches targeting miR-494 or its targets may be attractive candidates for inhibiting ER stress dependent pathologies in human disease.
2021-09-09 | PXD019992 | Pride
Project description:Investigation of whole genome gene expression level changes in miR-139-5p mimic-treated EC109 cells, compared to the scrambled negative controls. A four chip study using total RNA recovered from two separate cultures of miR-139-5p mimic-transfected EC109 cells and two separate cultures of scrambled negative control-transfected EC109 cells. Each chip measures the expression level of 44,049 genes from human esophageal cancer cell EC109 with three 60-mer probe pairs per gene.
2012-11-27 | E-GEOD-42486 | biostudies-arrayexpress
Project description:Next to genetic alterations, it is being recognized that the cellular environment also acts as a major determinant in onset and progression of disease. In cases where different cell types contribute to the final disease outcome, this imposes environmental challenges as different cell types likely differ in their extracellular dependencies. A number of skin diseases, including psoriasis is characterized by a combination of keratinocyte hyperproliferation and immune cell activation. Activation of immune cells involves increased glucose consumption thereby intrinsicly limiting glucose availability for other cell types. Thus, these type of skin diseases require metabolic adaptations that enable coexistence between hyperproliferative keratinocytes and activated immune cells in a nutrient-limited environment. Hsa-microRNA-31-5p (miR-31) is highly expressed in keratinocytes within the psoriatic skin. Here we show that miR-31 expression in keratinocytes is induced by limited glucose availability and enables increased survival of keratinocytes under limiting glucose conditions, by increasing glutamine metabolism. In addition, miR-31 induced glutamine metabolism results in secretion of specific metabolites (aspartate and glutamate) but also secretion of immuno-modulatory factors. We show that this miR-31-induced secretory phenotype is sufficient to induce Th17 cell differentiation, a hallmark of psoriasis. Inhibition of glutaminase (GLS) using CB-839 impedes miR31-induced metabolic rewiring and secretion of immuno-modulatory factors. Concordantly, pharmacological targeting of GLS alleviated psoriasis pathology in a mouse model of psoriasis. Together our data illustrate an emerging concept of metabolic interaction across cell compartments that characterizes disease development, which can be employed to design effective treatment options for disease, as shown here for psoriasis.
2023-02-06 | PXD029030 | Pride
Project description:In the largest published genome-wide association study (GWAS) of schizophrenia to date (PGC1), the most significant association (P = 1.6 X 10-11) was observed at an intronic variant (rs1625579) within the MIR137 host gene (MIR137HG). In this study we have performed genome-wide RNA profiling of a human foetal neural progenitor cell line following miR-137 manipulation, in order to identify gene expression changes through which genetic variation at the MIR137HG locus could confer susceptibility to schizophrenia. Total RNA extracted from human neural progenitor cells manipulated with either mir137 inhibitor or mimic. 4 replicates per group. Genome wide transcript levels were then measured using gene expression microarrays.
2014-02-10 | E-GEOD-49793 | biostudies-arrayexpress
Project description:These experiments were conducted as part of a study to derive the targets of miRNAs (See also E-MTAB-418). Two independent BayGenomics mouse embryonic stem cell lines (XH157 and XG058), each bearing a gene trap between exons 9 and 10 of the Dgcr8 locus (ENSMUST00000115633, Ensembl v53) were further mutagenised by the targetted insertion of a second Dgcr8 gene trap cassette. Consequently two independent heterozygous and two independent homozygous mutant Dgcr8 cells were derived (Dgcr8tm1,gt1/+, Dgcr8tm1,gt2/+, Dgcr8gt1/tm1 and Dgcr8gt2/tm1). Subsequently individual miRNA mimics were reintroduced into the Dgcr8-depleted background. In this set of experiments, cells were allowed to recover for 10 hours. The effect of the miRNA on the mRNA expression of the cells was assessed through the comparison of the expression profile of the transfected cells to that of cells transfected with a control mimic, which had recovered over the same period. This allows the roles of individual miRNAs to be investigated.
2012-08-20 | E-MTAB-968 | biostudies-arrayexpress
Project description:The product of genomic loci coding for micro RNAs (miRNAs) produce many isoforms (isomiRs). IsomiRs differing at their 5’ end have different seed regions and therefore are expected to target different genes. We used microarrays to study the effect of different isomiRs in the context of breast cancer. The product of genomic loci coding for micro RNAs (miRNAs) produce many isoforms (isomiRs). IsomiRs differing at their 5’ end have different seed regions and therefore are expected to target different genes. We used microarrays to study the effect of different isomiRs in the context of breast cancer. Breast cancer MDA-MB-231 cells were cultured and were subject to a negative control treatment or transfected with one of the three selected isomiRs: the archetype miRNA, the miR-183-5p|2|-2| or the miR-183-5p|+2|+2| isomiR. Each treatment was done in triplicate. RNA was extracted and hybridized on Affymetrix microarrays.
2015-09-23 | E-GEOD-71950 | biostudies-arrayexpress
Project description:Alzheimer’s disease (AD) is a serious neurodegenerative disease in which miRNAs have been linked to its pathogenesis. miR-603 is a primate-specific miRNA. Through ADNI data analysis, we found a SNP rs11014002 in pre-miR-603 which promotes the biogenesis of mature miR-603 is associated with AD risk. We further identified that LRPAP1, a protein which antagonizes the function of LRP1 in Aβ clearance and AD susceptibility, is a target gene of miR-603. Moreover, overexpression of miR-603 increased the protein level of LRP1, suggesting the protective role of miR-603 in AD. Both significant increase and loss of regulatory function of miR-603 hint the existence of a compensatory mechanism in hippocampus of AD subjects. Furthermore, we found that miR-603 could directly downregulate E2F1 and prevent cells from H2O2 induced-apoptosis. This work provides the first evidence that miR-603 may modulate AD susceptibility and the SNP rs11014002 (T-carrier genotype) might be a protective factor for AD. There are two groups: Negative Control and miR-603 overexpression. We performed experiments on HEK293 cell and Hela cell.
2015-05-18 | E-GEOD-68987 | biostudies-arrayexpress
Project description:miR-145 is downregulated in multiple cancers. The introduction of miR-145 could alleviate the tumor burden in the pancreatic cancer mouse model. However, how miR-145 mediates the tumor suppression is still an open question. In this study, we aimed to identify the targets of miR-145 using a SILAC approach.
2014-10-28 | PXD001260 | Pride
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2014-01-30 | E-GEOD-54494 | biostudies-arrayexpress