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This essay examines recent advances in the use of psychostimulant use on redox-imbalance-induced DNA methylation to create novel epigenetics-based early interventions. Conclusions: In various research models stimulated by psychostimulants and opioids, degradation of DNA methylation signatures in neurological disorders has been demonstrated, indicating widespread involvement of epigenetic shifts in DNA methylation signatures in neurological disorders. This review summarizes the need for more research and experimental analyses of DNA-methylation-based drugs that may help to determine the relationship between psychostimulant use and oxidative stress or redox-linked metabolic recalibration, which may help to clarify neuronal impairments.
Source link: https://europepmc.org/article/MED/35227168
Heterochromatin is the most compacted form of chromatin with different condensation characteristics characterized by high DNA methylation. MeCP2 is mostly known as a DNA methylation reader, but it has also been described as a heterochromatin designer. We'll explore the mechanism of MeCP2-driven heterochromatin formation and dynamics by combining liquid-liquid phase separation analysis and single-molecule tracking with quantification of local MeCP2 concentrations in vitro and in vivo. Crowded environments and DNA help MeCP2 LLPS and slow down MeCP2 mobility.
Source link: https://europepmc.org/article/MED/35156529
Many cancers, including head and neck squamous cell carcinomas, are under scrutiny by the tumor necrosis factor receptor superfamily, which are all under scrutiny as targets for immunotherapy. The Cancer Genome Atlas Research Network performed broad comparative studies of DNA methylation of 46 CpG sites within the GITR/OX40 gene locus in head and neck squamous cell carcinomas and normal adjacent tissues. In addition, we investigated methylation levels in HPV-positive and HPV-negative cell lines and in isolated monocytes, granulocytes, CD8+, and CD4+ T cells from healthy donors. We found significant methylation differences between normal adjacent and tumor tissues, between HPV-positive and HPV-negative tumors, within tumor and immune cells, as well as strong correlations between tumor and immune cells, as well as strong correlations between methylation and mRNA expression. CpG methylation has been shown to be highly correlated with overall survival, signatures of immune cell infiltrates, an interferon-like signature, and mutational load.
Source link: https://europepmc.org/article/MED/34908008
Cellular carcinoma cells and immortalized human hepatocyte cells were then analyzed for their cytotoxic activity on hepatocellular carcinoma cells and immortalized human hepatocyte cells. In addition, its effect on Hep3B's global DNA methylation inhibition was also determined. With an IC 50 = 109. 7 0. 9 % 0. 9 M, we found that the cinnamic derivatives 11-14 and 20-22 were more potent than the free caffeic acid, being methyl 3,4-dihydroxycinammate the most active with an IC 50 = 109. 7 0. 8 mm. One of the molecular docking of 21 and 14 has been found to partially adhere to the DNA methyltransferase 1 pocket in SAH-binding pocket.
Source link: https://europepmc.org/article/MED/35451561
As an indicator of lung cell death, lung-derived cell-free DNA methylation patterns in Lung epithelium-specific DNA methylation patterns can possibly reveal the presence of lung-derived cell-free DNA in blood. We developed a PCR-sequencing assay that determined the methylation status of 17 loci with lung-specific methylation patterns and used it to analyze lung-derived cfDNA in healthy volunteers and patients with lung disease. A significant rise in lung cfDNA levels in blood is seen in people with advanced lung cancer. In the plasma of those later diagnosed with lung cancer and to a lesser extent in those with other respiratory disorders, bronchoscopy has been found in the plasma of those undergoing bronchoscopy, lung-derived cfDNA. In patients with acute obstructive pulmonary disease with acute exacerbation compared to patients with stable disease, Lung cfDNA is also elevated in patients with acute exacerbation of chronic pulmonary disease (LT) and mortality in these patients, which is also associated with future exacerbation and mortality in these patients.
Source link: https://europepmc.org/article/MED/35450968
Individuals with latent tuberculosis infection were considered a substantial reservoir of cases of active tuberculosis. To improve LTBI management, biomarkers and devices are urgently needed for detecting and ruling out active TB in a fast and cost-effective manner. DNA methylation results were retrospectively found in an open-label controlled trial designed to find short-course LTBI treatment regimens, and they were also discovered to look for potential biomarkers that could discriminate active TB from LTBI. The Infinium MethylationEPIC BeadChip array was used to determine genomewide DNA methylation levels for 15 people with active TB and 15 healthy LTBI controls who remained healthy, as well as 15 LTBI controls who did not develop active TB. Our preliminary findings show that the DNA methylation level may be a useful diagnostic biomarker for separating active disease in LTBI testing. IMPORTANCE Approximately half of the world population had been infected with Mycobacterium tuberculosis, and about 5 to 10% of these people may have active disease in their lifetimes. Preventive treatment has been shown to prevent 60 to 90 percent of high-risk LTBIs from developing active disease, as a key component of the "end TB framework. " Before initiating intervention, developing new TB screening kits based on blood-based biomarkers, which may help to identify and rule out active TB from LTBI are a prerequisite. We tried to identify potential DNA methylation diagnostic biomarkers by retrospectively determining DNA methylation profiles pre- and post-TB diagnosis. The preliminary findings revealed new insight into determining the DNA methylation level as a potential way to distinguish TB from LTBI.
Source link: https://europepmc.org/article/MED/35446152
We investigated the interplay between TF binding and DNA methylation in 19 cancer types by combining DNA methylation arrays and gene expression data with TF binding sites. We performed emQTL tests in each cancer type and discovered 13 TFs whose expression levels were correlated with local DNA methylation patterns around their binding sites in at least two cancer types. Both cancer and tumor-infiltrating cells were found in modulation of DNA methylation associated with TF binding at cis-regulatory zones governing immune- and cancer-associated pathways, supporting the emQTL signals, which were shown to be derived from both cancer and tumor-infiltrating cells. We also reported physical interactions between FOXA1 and TET1 and TET2 in vitro and in vivo in MCF-7 cells, providing further evidence for FOXA1's attraction of TET1 and TET2 to local demethylation in cancer cells.
Source link: https://europepmc.org/article/MED/35440061
Serrated Polyposis Syndrome is a risk factor for colorectal cancer. Intense promoter hypermethylation is a common molecular finding in the serrated pathway, and it can be present in normal mucosa predisposing to the formation of serrated lesions. Using the 850K BeadChip Technology, researchers were able to identify novel biomarkers for SPS, fresh frozen samples of normal mucosa from 50 patients with SPS and 19 healthy individuals were analyzed to determine novel biomarkers for SPS, and healthy individuals with SPS. HLA-F, SLFN12, and HLA-DMA expression levels were significantly different between SPS patients and healthy people, and they were closely linked to the corresponding DMR's methylation status. CpGs were also present in serrated lesions, which led to significant hypermethylation of CpGs in the gene body of HLA-F. Multiple differentially methylated CpGs were discovered in normal mucosa from SPS patients by Epigenome-wide methylation profiling. HLA-F's gene body is a novel biomarker candidate for SPS due to significant hypermethylation of the gene body.
Source link: https://europepmc.org/article/MED/35447336
Background Methylated SDC2 has been used as a diagnostic tool for human colorectal cancer diagnosis, but noninvasive stool DNA-based methylation testing has also emerged as a new method for detecting CRC. The objective of this research was to determine the clinical results of stool DNA-based SDC2 methylation test by a new qPCR detection reagent for early detection of CRC. In this research, two differently methylated regions in SDC2 CpG islands for the detection of CRC were used. Results The test kit was able to detect methylated SDC2 in stool DNA samples with concentrations as low as 90 copies/L in 99 percent of replicates. Conclusions This research established the ability of stool DNA-based SDC2 methylation test for early screening of CRC, and the simultaneous detection of two SDC2 fragments of SDC2 gene could increase detection sensitivity.
Source link: https://europepmc.org/article/MED/35436855
5-aza-2'-deoxycytidine, a chemotherapeutic DNA methyltransferase inhibitor widely used to treat myelodysplastic syndrome and acute myeloid leukemias. However, we previously reported However, we previously reported contradictory effects on DNA methylation by decitabine in somatic tissues. We chose to investigate its long-term effects here due to the dangers that DNA methylation in reproductive organs from even short courses of decitabine in reproductive age humans. Mice were treated with two clinically appropriate doses of decitabine for seven weeks, and DNA methylation was determined within female reproductive tract tissues. We found methylated cytosines within the ovary to be the least sensitive to decitabine exposure at both doses, although the uterus and the oviduct showed elevated 5mC dysregulation, despite being surprisingly sensitive to hypermethylation at the 0. 35 mg/kg dose. Overall, our findings indicate that decitabine use leads to an epigenetic alteration of DNA methylation in female reproductive tissues.
Source link: https://europepmc.org/article/PPR/PPR483306
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