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Anti-proliferative tumor suppressor-like activity of mir-9 overexpression and identification of novel mir-9 targets by trancription profiling in breast cancer cells

ABSTRACT: Investigation of genome-wide effects (transcriptome profiling) and direct targets of mir-9 in MCF-7 cells transfected with mir-9 in two dosages (1X and 2X) Following transfections of mir-9 or control miRNA mimics, total RNA was isolated and microarray profiling was performed.

ORGANISM(S): Homo sapiens

SUBMITTER: Charles Spillane

PROVIDER: E-GEOD-33952 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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MicroRNA-9 inhibition of cell proliferation and identification of novel miR-9 targets by transcriptome profiling in breast cancer cells.

Selcuklu S Duygu SD Donoghue Mark T A MT Rehmet Kristina K de Souza Gomes Matheus M Fort Antoine A Kovvuru Prasad P Muniyappa Mohan K MK Kerin Michael J MJ Enright Anton J AJ Spillane Charles C

The Journal of biological chemistry 20120702 35

Although underexpression of miR-9 in cancer cells is reported in many cancer types, it is currently difficult to classify miR-9 as a tumor suppressor or an oncomir. We demonstrate that miR-9 expression is down-regulated in MCF-7 and MDA-MB-231 breast cancer cells compared with MCF-10-2A normal breast cell line. Increasing miR-9 expression levels in breast cancer cells induced anti-proliferative, anti-invasive, and pro-apoptotic activity. In addition, microarray profiling of the transcriptome of ...[more]

PMID: 22761433

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Anti-proliferative tumor suppressor-like activity of mir-9 overexpression and identification of novel mir-9 targets by trancription profiling in breast cancer cells

Project description:Investigation of genome-wide effects (transcriptome profiling) and direct targets of mir-9 in MCF-7 cells transfected with mir-9 in two dosages (1X and 2X)

2012-09-04 | GSE33952 | GEO

proteomic effects of mIR-877-3p in cervical cancer

Project description:A subcellular proteomic workflow was carried out with three biological replicates in each experimental condition, using MOCK, NC- and anti-miR-877-transfections in C-33A and SiHa cells.

2021-09-08 | PXD014993 | Pride

MicroRNAs in the miR-106b family regulate p21/CDKN1A and promote cell cycle progression.

Project description:microRNAs in the miR-106b family are overexpressed in multiple tumor types and are correlated with the expression of genes that regulate the cell cycle. Consistent with these observations, miR-106b family gain of function promotes cell cycle progression, whereas loss of function reverses this phenotype. Microarray profiling uncovers multiple targets of the family, including the cyclin-dependent kinase inhibitor p21/CDKN1A. We show that p21 is a direct target of miR-106b and that its silencing plays a key role in miR-106b-induced cell cycle phenotypes. We also show that miR-106b overrides a doxorubicin-induced DNA damage checkpoint. Thus, miR-106b family members contribute to tumor cell proliferation in part by regulating cell cycle progression and by modulating checkpoint functions. HCT116 Dicerex5 cells were transfected with microRNAs in six-well plates, and RNA was isolated 10 h after transfection. Transcripts containing the miR-106b family hexamers in their 3' UTRs were identified. By microarray analysis, 103 transcripts that contained miR-106b family complementary hexamers in their 3' UTRs were down-regulated by miR-106b, miR-106a, miR-20b, and miR-17-5p within 10 h of transfection.

2010-06-23 | E-GEOD-14831 | biostudies-arrayexpress

A miR-494 dependent feedback loop regulates ER stress (ANAN-376 Project)

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

Identification of miR-145 targets using SILAC

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

Identification of miR-16/29 targets in adipocytes by LC-MSMS

Project description:Cancer cachexia is a multifactorial metabolic syndrome defined by the rapid loss of skeletal muscle mass and the loss of fat mass. Up 80% of cancer patients at the late stage with cachexia suffer from progressive atrophy of adipose tissue. Unlike studies on skeletal muscle wasting, there is limited research on fat loss in cachexia. It was noted that most patients suffer from fat loss as cancer progress. Fat loss precedes muscle loss, is associated with shorter survival, and is variable to timing and intensity in various cancer populations. Increased lipolysis may be the leading cause of fat loss in cancer cachexia. miRNAs are a class of non-coding RNAs of 19~25 nucleotides that regulate gene silencing by interacting with the 3’ untranslated region (UTR) of target mRNA to cause mRNA degradation and translational repression. miRNAs play multifaceted roles in pancreatic cancer proliferation, survival, metastasis, and chemoresistance. Aberrant expression of miRNA in circulating exosomes may play potential roles in modulating fat loss in cancer cachexia. We identified 2 miRNAs, miR-16 and miR-29, which have 2-fold higher expression existed in at PDAC cells. To explore which genes in adipogenesis and lipolysis were directly affected by miR-16-5p or/and miR-29a-3p, we analyzed the targets which were down-regulated in both miR-16-5p and miR-29a-3p-transfected 3T3-L1 cells by mass analysis.

2024-06-13 | PXD037998 | Pride

Identification of miR-16/29 targets in adipocytes by LC-MSMS

2024-06-13 | PXD037862 | Pride

Transcriptional consequences of manipulating the candidate schizophrenia susceptibility gene miR-137 in human neural progenitor cells

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

Hsa-miR-31-5p controls a metabolic switch in psoriatic keratinocytes that identifies therapeutic intervention

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

MicroRNAs may indirectly regulate other microRNAs

Project description:MicroRNAs (miRNAs) are a class of regulatory RNAs that control the expression of genes critical to cell function. Ectopic expression of miRNAs has been shown to result in genome-wide changes in patterns of gene expression. While the reasons for these global alterations in gene expression patterns have been attributed to the ability of miRNAs to target multiple genes, and/or to induce indirect effects downstream of target genes, the molecular basis of indirect effects of miRNA regulation remains poorly understood. In this study, we demonstrate the potential of miRNAs to regulate other miRNAs. Using miRNA microarray analysis, we show that over 70 different miRNAs are differentially expressed ( M-bM-^IM-%1.4 fold, FDR M-bM-^IM-$ 5%) in human ovarian cancer cells after transfection with a single miRNA (miR-7). We present evidence that a major component of miR-7-induced changes in levels of miRNAs is the indirect consequence of miR-7-mediated alterations in levels of protein-coding genes (e.g., transcription and splicing factors) that exert trans-regulatory control on miRNAs. HEY cells were transfected with either hsa-miR-7 (2 biological replicates) or a negative control miRNA, miR-NC (2 biological replicates), and then grown in 6-well plates for ~48 hours. The difference in miRNA expression pattern between the miR-7-transfected cells and the miR-NC-transfected cells was determined using an Affymetrix GeneChip miRNA Array.

2012-04-08 | E-GEOD-29129 | biostudies-arrayexpress

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