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Methylation gene promoter hypermethylation - Crossref

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Last Updated: 27 January 2022

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Decreased DNA methylation at promoters and gene-specific neuronal hypermethylation in the prefrontal cortex of patients with bipolar disorder

Abstract Bipolar disorder is a serious mental disorder characterized by repeated mood swings and is difficult to describe. Neuronal and nonneuronal nuclei were determined in the prefrontal cortex of patients with BD and controls, according to a survey by the University of promoter-wide DNA methylation analysis. In both cell types of the BD patients and controls, DNA methylation in promoters was reduced in both cell types and patients compared to the controls. The effect of drugs, neuroblastoma cells cultured in therapeutic concentrations of three different mood stabilizers was determined. We found that up to 37. 9% of DMRs detected in BD closely with mood stabilizer-induced DMRs. Interestingly, mood stabilizer-induced DMRs in BD went in the opposite direction of DMR changes in BD, suggesting the therapeutic benefits of mood stabilizers on DNA methylation. DNMT3B was overexpressed in BD by qPCR analysis of ten DNA methylation-related genes, and we discovered that DNMT3B was overexpressed in BD.

Source link: https://doi.org/10.1101/2020.12.10.20246405


Vegfa promoter gene hypermethylation at HIF1α binding site is an early contributor to CKD progression after renal ischemia

After Acute Kidney Injury, Chronic hypoxia is a key contributor to Chronic Kidney Disease. However, the causal connection between the acute insult and impaired renal response to hypoxia remains uncertain. At the first month post-ischemia, there was a twofold significant rise in oxidative stress and decrease in global DNA methylation, which was maintained throughout the study. In the first and second months post-ischemia, Hif1 and Vegfa expression were depressed, followed by Hif1 and Vegfa expression, and Hif1 and Vegfa expression were depressed, and then Hif1 but not Vegfa expression was restored, but not Vegfa expression was restored. Interestingly, hypermethylation of the Vegfa promoter gene at the HIF1 binding site was discovered at the HIF1 binding site during the early stages of the CKD path.

Source link: https://doi.org/10.1038/s41598-021-88000-5


Abnormal promoter DNA hypermethylation of the integrin, nidogen, and dystroglycan genes in breast cancer

Cell transmembrane receptors and extracellular matrix components play a central role in controlling cell proliferation and encouraging coordinated integration of cells in the tissue structures. DNA methylation has been determined in normal breast tissues and breast carcinomas, in eight integrin genes, two nidogen genes, and the dystroglycan gene. The frequencies of abnormal promoter hypermethylation in BC were 13% for ITGA1, 31% for NID1, 49% for ITGA9, 41% for NID1, and 41% for NID2, with 43% for ITGA1, 49% for NID1, 41% for NID1, and 41% for NID2, respectively. The HER2 and integrin 4 receptors' simultaneous presence of both HER2 and integrin 4 receptors is not helpful to tumor cells, according to a strong correlation of abnormal ITGA4 hypermethylation with the HER2 positive tumors.

Source link: https://doi.org/10.1038/s41598-021-81851-y


Deciphering Promoter Hypermethylation of Genes Encoding for RASSF/Hippo Pathway Reveals the Poor Prognostic Factor of RASSF2 Gene Silencing in Colon Cancers

In a single-center retrospective cohort of 229 patients treated for colon cancers, the aim of this report was to determine the frequency of promoter hypermethylation of the genes encoding the Ras associated domain family/Hippo pathway, as well as the effects on overall and progression-free survival. We found that colon cancer's RASSF/Hippo pathway to be largely silenced, especially RASSF2. One RASSF/Hippo family member's hypermethylation of at least two RASSF/Hippo promotors was by no means exclusive to the others, as the hypermethylation of at least two RASSF/Hippo members was in no way unique from the others. When the RASSF2 promoter was hypermethylated, survival tests revealed a significantly poorer overall survival of patients. On univariate analysis, the median OS was 53. 5 months for patients with colon cancer with a hypermethylated RASSF2 promoter rather than a placebo.

Source link: https://doi.org/10.3390/cancers13235957


Correlation between Promoter Hypermethylation of the O6-Methylguanine-Deoxyribonucleic Acid Methyltransferase Gene and Prognosis in Patients with High-grade Astrocytic Tumors Treated with Surgery, Radiotherapy, and 1-(4-Amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea-based Chemotherapy

We investigated whether MGMT promoter hypermethylation is related to prognosis in patients with high-grade astrocytic tumors treated uniformly with surgery, radiotherapy, and 1-methyl-3-hydroxysourea based chemotherapy. RESULTS MGMT promoter hypermethylation was detected in 19 of 42 of 42 AA patients and 33 of 74 GBM patients. CONCLUSION & MISION CONCLUSION Our results show that MGMT promoter hypermethylation is associated with longer life span in patients with AA who were treated with surgery, radiotherapy, and ACNU-based chemotherapy but not in patients with GBM.

Source link: https://doi.org/10.1227/01.neu.0000103422.51382.99


79696 Reversible DNA Hypermethylation of the Interleukin-15 Promoter Induces IL-15 Expression, Drives the Pathogenesis of T-Cell Large Granular Lymphocytic Leukemia (T-LGLL) and Provides a Therapeutic Approach Using 5-Azacitidine

ABSTRACT IMPACT: This research reports the methylome in patients with T-LGLL for the first time, focusing on the IL-15 promoter, and it clearly shows that 5-azacytidine reduces T-cell production leading to T-cell death in T-LGLL patients. These findings support a translational clinical trial in T-LGLL, which will begin accrual in 2021, with few treatment options owing to overexpression of IL-15. In a translational trial, we intend to investigate the effect of 5-aza in vitro on IL-15 levels and the IL-15 promoter, and the IL-15 promoter. POPULATION OF T-LGLL: We sorted T-LGLL patients and normal donor samples for CD3+/CD8+/CD5-/dim for T-LGLL immunophenotype, phenotypes. Using reduced representation bisulfite and RNA sequencing, we analyzed DNA methylation and gene expression profiling and established differential methylation and gene expression using 1-way ANOVA analysis. Next, we analyzed IL-15 gene expression in MOTN-1 cells treated with 5-Aza versus MOTN-1 with control using western immunoblot. We finally exposed MOTN-1 cells to a new IL-15 inhibitor, IBI-15, and tested cell viability against MOTN-1 cells exposed to an inactive control. A dose-dependent decrease in the viability of T-LGLL cells was observed in MOTN-1 cells treated in vitro with 5-Aza at 24 and 48 hours, from 100% to 48 percent, p=0. 037. Inhibition of the IL-15 promoter by 5-aza results in down-regulation of the IL-15 gene transcript, which is sufficient to cause T-LGLL cell death.

Source link: https://doi.org/10.1017/cts.2021.638


Decreased DNA methylation at promoters and gene-specific neuronal hypermethylation in the prefrontal cortex of patients with bipolar disorder

Abstract Bipolar disorder is a serious mental disorder characterized by repeated mood swings. Neuronal and nonneuronal nuclei were found in the prefrontal cortex of patients with BD and controls, allowing for translation-wide DNA methylation analysis. In both cell types in the BD patients, we observed decreased DNA methylation at promoters. To determine the effects of medications, neuroblastoma cells were cultured in therapeutic concentrations of three mood stabilizers. DMRs detected in BD related to mood stabilizer-induced DMRs, which we found in a significant way. Interestingly, mood stabilizer-induced DMRs tended in the opposite direction of DMR evolutions, suggesting the therapeutic benefits of mood stabilizers. In another GWAS of BD, we also discovered significant enrichment of neuronal DMRs in the loci. DNMT3B was overexpressed in BD, according to a study by DNA methylation-related genes.

Source link: https://doi.org/10.1038/s41380-021-01079-0


Promoter Hypermethylation Promotes the Binding of Transcription Factor NFATc1, Triggering Oncogenic Gene Activation in Pancreatic Cancer

Transcript factors have been suggested that transcription factors could bind specifically to methylated promoters and trigger transcription. We investigated this more closely for pancreatic ductal carcinomacinoma and examined some cases in more detail. In comparison to healthy tissue, PDAC's 2% of tightly controlled genes exhibited higher transcription related to promoter hypermethylation in comparison to healthy tissues. Further research established that direct regulation of ALDH1A3 transcription by NFATc1 promoter binding in a methylation-dependent process, providing insight into the oncogenic role of transcription activation in PDAC, which is aided by DNA methylation.

Source link: https://doi.org/10.3390/cancers13184569

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions