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DNA Methyltransferase Inhibition Upregulates the Costimulatory Molecule ICAM-1 and the Immunogenic Phenotype of Melanoma Cells.
JID Innov
March 2025
Department of Dermatology, University Hospital of Zurich, University of Zurich, Schlieren, Switzerland.
In cutaneous melanoma, epigenetic dysregulation is implicated in drug resistance and tumor immune escape. However, the epigenetic mechanisms that influence immune escape remain poorly understood. To elucidate how epigenetic dysregulation alters the expression of surface proteins that may be involved in drug targeting and immune escape, we performed a 3-dimensional surfaceome screen in primary melanoma cultures and identified the DNA-methyltransferase inhibitor decitabine as significantly upregulating the costimulatory molecule ICAM-1.
View Article and Find Full Text PDFThe methyl-CpG binding domain 2 regulates peptidylarginine deiminase 4 expression and promotes neutrophil extracellular trap formation via the Janus kinase 2 signaling pathway in experimental severe asthma.
Ann Med
December 2025
Department of Pulmonary and Critical Care Medicine, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, Hunan, China.
Objective: The prognosis for severe asthma is poor, and the current treatment options are limited. The methyl-CpG binding domain protein 2 (MBD2) participates in neutrophil-mediated severe asthma through epigenetic regulation. Neutrophil extracellular traps (NETs) play a critical role in the pathogenesis of severe asthma.
View Article and Find Full Text PDFMethyl-CpG-Binding Domain Protein 2 is Involved in Th17 Cell Differentiation by Negatively Regulating Leptin Expression.
Curr Mol Med
January 2025
Hainan Medical University, Guilin 570100, Xueyuan Road No.3, Haikou, China.
Background: Among Th lineages from naïve CD4+T cells, Th17 cells producing IL-17 are strongly related to the pathogenesis of neutrophilic asthma. Leptin is involved in inflammation and immunity. Little is known about MBD2's epigenetic regulation in CD4+T cell differentiation.
View Article and Find Full Text PDFFOXS1, frequently inactivated by promoter methylation, inhibited colorectal cancer cell growth by promoting TGFBI degradation through autophagy-lysosome pathway.
J Adv Res
January 2025
Biomedical Research Center, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou 310016 Zhejiang, China; Department of Pathology, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou 310016 Zhejiang, China. Electronic address:
Introduction: Tumor suppressor gene (TSG) inactivation by epigenetic modifications contributes to the carcinogenesis and progression of colorectal cancer (CRC). Expression profiling and CpG methylomics revealed that a forkhead-box transcriptional factor, FOXS1, is downregulated and methylated in CRC.
Objectives: To assess the biological functions and underlying mechanisms of FOXS1 in colorectal cancer.
Tissue nanotransfection-based endothelial PLCγ2-targeted epigenetic gene editing in vivo rescues perfusion and diabetic ischemic wound healing.
Mol Ther
January 2025
Department of Surgery, McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA 15219, United States; Department of Surgery, Indiana Center for Regenerative Medicine and Engineering, Indiana University School of Medicine, Indianapolis, IN 46202, United States. Electronic address:
Diabetic wounds are complicated by underlying peripheral vasculopathy. Reliance on vascular endothelial growth factor (VEGF) therapy to improve perfusion makes logical sense, yet clinical study outcomes on rescuing diabetic wound vascularization have yielded disappointing results. Our previous work has identified that low endothelial phospholipase Cγ2 (PLCγ2) expression hinders the therapeutic effect of VEGF on the diabetic ischemic limb.
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