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DNMT1 inhibition improves the activity of memory-like natural killer cells by enhancing the level of autophagy.
Mol Biol Rep
December 2024
Yunnan Key Laboratory of Laboratory Medicine, Yunnan Province Clinical Research Center for Laboratory Medicine, Department of Clinical Laboratory, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650032, China.
Background: Acute myeloid leukemia (AML) is a common hematological tumor, but it is difficult to treat. DNMT1 is a DNA methyltransferase whose main function is to maintain stable DNA methylation during the DNA replication process. DNMT1 also plays an important role in AML, but its function in cytokine-induced memory-like natural killer (CIML NK) cell activity remains unclear.
View Article and Find Full Text PDFPrognostic value of ubiquitination-related differentially expressed genes in esophageal squamous cell carcinoma: a comprehensive analysis and future directions.
J Thorac Dis
November 2024
Department of Radiation Oncology, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, China.
Background: Esophageal squamous cell carcinoma (ESCC) represents a considerable health challenge, primarily due to its poor prognosis and the limited availability of effective therapeutic interventions. Ubiquitination, a vital post-translational modification, is integral to cellular regulation; nonetheless, its role in ESCC has not been thoroughly explored. This study aims to identify ubiquitination-related differentially expressed genes (URDEGs) that possess prognostic significance in the context of ESCC.
View Article and Find Full Text PDFAsperosaponin VI inhibition of DNMT alleviates GPX4 suppression-mediated osteoblast ferroptosis and diabetic osteoporosis.
J Adv Res
December 2024
Department of Orthopaedics, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, 98 West Nantong Road, Yangzhou 225001, China; Department of Orthopaedics, Northern Jiangsu People's Hospital, 98 West Nantong Road, Yangzhou 225001, China; The Yangzhou School of Clinical Medicine of Dalian Medical University, 98 West Nantong Road, Yangzhou 225001, China; Northern Jiangsu People's Hospital, Clinical Teaching Hospital of Medical School, Nanjing University, 98 West Nantong Road, Yangzhou 225001, China. Electronic address:
Introduction: Diabetic osteoporosis (DOP) is an insidious complication of diabetes with limited therapeutic options. DOP is pathologically associated with various types of regulated cell death, but the precise role of ferroptosis in the process remains poorly understood. Asperosaponin VI (AVI), known for its clinical efficacy in treating bone fractures and osteoporosis, may exert its osteoprotective effects through mechanisms involving ferroptosis, however this has not been established.
View Article and Find Full Text PDFTFPI2 hypermethylation promotes diabetic atherosclerosis progression through the Ap2α/PPARγ axis.
J Mol Cell Cardiol
December 2024
Department of Cardiology, The Affiliated Hospital of Qingdao University, 16 Jiangsu Road, Qingdao 266003, Shandong, China. Electronic address:
Article Synopsis
- - Diabetes significantly increases the risk of atherosclerosis, causing serious cardiovascular problems, with research showing that the protein TFPI2 is expressed at lower levels in atherosclerotic plaques of diabetic patients.
- - Experiments demonstrated that knocking down TFPI2 in non-diabetic mice led to more severe plaque buildup and increased inflammation, while boosting TFPI2 in diabetic mice improved plaque stability and promoted beneficial M2 macrophage activity.
- - The study reveals that the interaction between TFPI2 and a transcription factor called AP-2α is essential for regulating inflammation and plaque stability in diabetes, suggesting that targeting this pathway could be a novel way to treat diabetes-related cardiovascular diseases.
DNMT1-Dependent DNA Methylation of lncRNA FTX Inhibits the Ferroptosis of Hepatocellular Carcinoma.
Crit Rev Eukaryot Gene Expr
December 2024
Article Synopsis
- Hepatocellular carcinoma (HCC) is a highly aggressive tumor, and long non-coding RNAs (lncRNAs) play a significant role in its development, particularly the lncRNA FTX.
- The study found that FTX is less active in HCC patients, leading to poorer outcomes, and that its expression is reduced due to DNA methylation by DNMT1.
- Enhancing FTX levels triggers cell death (ferroptosis) in HCC cells by regulating the miR-374b-3p/TFRC pathway, suggesting the DNMT1/FTX/miR-374b-3p/TFRC pathway could be a promising target for new therapies in HCC
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