MiR expression microarray analysis on M2 macrophages treated with epigenetic modifiers
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ABSTRACT:
ORGANISM(S): Mus musculus synthetic construct
PROVIDER: GSE218160 | GEO | 2022/11/17
REPOSITORIES: GEO
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Project description:The innate immune signaling pathway plays a crucial role in the recognition and early response to pathogens associated with disease. Genetic analysis has been unable to completely account for individual variability in the strength of the innate immune response. The aim of this study was to determine the role of the epigenetic markers (DNA methylation or histone acetylation) in controlling bovine gene expression in relation to the response to lipopolysaccharide (LPS). To determine the impact epigenetics may have in controlling innate immunity, dermal fibroblasts from fifteen dairy heifers having previously displayed a differential response to LPS were exposed to 5-aza-2’-deoxyctidine (AZA) and trichostatin A (TSA); de-methylating and hyper-acetylating agents, respectively. The AZA-TSA
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Project description:Purpose: The major aim of this study was to investigate the role of DNA methylation (referred to as methylation) on microRNA (miRNA) silencing in non-small cell lung cancers (NSCLC). Experimental Design: We performed microarray expression analyses of 856 miRNAs in NSCLC A549 cells before and after treatment with the DNA methyltransferase inhibitor 5-aza-2´-deoxycytidine (Aza-dC) and with a combination of Aza-dC and the histone deacetylase inhibitor trichostatin A. MiRNA methylation was determined in 11 NSCLC cell lines and in primary tumors and corresponding non-malignant lung tissue samples of 101 stage I-III NSCLC patients. Results: By comparing microarray data of untreated and drug treated A549 cells, we identified 33 miRNAs whose expression was upregulated after drug treatment and which are associated with a CpG island. Thirty (91%) of these miRNAs were found to be methylated in at least 1 of 11 NSCLC cell lines analysed. Moreover, miR-9-3 and miR-193a were found to be tumor-specifically methylated in NSCLC patients. We observed a shorter disease-free survival of miR-9-3 methylated lung squamous cell carcinoma (LSCC) patients compared to miR-9-3 unmethylated LSCC patients by multivariate analysis (HR = 3.8, 95% CI = 1.3 to 11.2, p = 0.017) and a shorter overall survival of miR-9-3 methylated LSCC patients compared to miR-9-3 unmethylated LSCC patients by univariate analysis (p = 0.013). Conclusions: Overall, our results suggest that methylation is an important mechanism for inactivation of certain miRNAs in NSCLCs and that miR-9-3 methylation may serve as a prognostic parameter in LSCC patients. MiRNA expression (LC Sciences, mirBASE12) was analyzed before and after treatment of A549 cells with 5-aza-2´-deoxycytidine (Aza-dC) and a combination of Aza-dC and trichostatin A (TSA). Experiments were performed in duplicates.
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