DNA and cell biology最新文献

{"title":"<i>In Vitro</i> Study of the Damaging Effects of the Fungicide Dithianon on DNA Structure by Spectroscopic Techniques.","authors":"Parvaneh Pakravan","doi":"10.1089/dna.2024.0158","DOIUrl":"10.1089/dna.2024.0158","url":null,"abstract":"<p><p>The common broad-spectrum protectant fungicide known as Dithianon is utilized in agriculture to manage pests; however, it could pose risks to human health. Dithianon may be associated with health problems due to its affinity for DNA. The interaction between Dithianon and calf thymus DNA (CT-DNA) was examined using UV-Vis absorption, fluorescence spectroscopy, and viscosity measurements with Neutral Red (NR) dye as a spectral probe in a physiological buffer. Dithianon, intercalated in DNA (K [DNA-Dithianon] = 2.3 × 10⁵ M^-1), causes the displacement of the NR dye from the NR-DNA complex. The binding constants (K_f), the number of binding sites (n ≈ 1), and thermodynamic parameters of the interaction of DNA-Dithianon were determined using the fluorescence quenching method at various temperatures. Dithianon's ability to intercalate in DNA base pairs was further supported by the variations in CT-DNA base stacking observed in circular dichroic spectrum measurements and the rise in viscosity of the CT-DNA solution. The interaction energy between Dithianon and the DNA was primarily due to hydrophobic Van der Waals interactions. This study offers a comprehensive understanding of how dithianon interacts with CT-DNA, providing insights into the toxic effects of the fungicide.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"421-435"},"PeriodicalIF":2.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144546631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Granzyme K, Regulated by the N6-Methyladenosine Methyltransferase Wilms' tumor 1-associate protein, Enhances Myocardial Infarction Injury.","authors":"Qing Lyu, Le Li","doi":"10.1089/dna.2025.0067","DOIUrl":"10.1089/dna.2025.0067","url":null,"abstract":"<p><p>Myocardial infarction (MI) is a major contributor to death in contemporary society, and this mechanism involves n6-methyladenosine (m⁶A) modification. In this study, we studied the m⁶A mechanisms involved in MI. For this purpose, an H9C2 cell MI model and MI rat model were developed. Cell Counting Kit-8 was applied to determine the effect of granzyme K (GZMK) differential expression on cell survival. In addition, 2,3,5-triphenyl tetrazolium chloride, hematoxylin-eosin, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining, and enzyme-linked immunosorbent assay were performed to determine the effect of GZMK differential expression on myocardial injury markers, apoptosis, and inflammatory factors. The m⁶A-modification effect between Wilms' tumor 1-associate protein (WTAP) and GZMK was detected via methylated RNA immunoprecipitation. The expression of WTAP and GZMK in MI model cardiomyocytes was measured by quantitative reverse transcription polymerase chain reaction and western blotting. WTAP and GZMK were found to be highly expressed in MI H9C2 cells. Moreover, GZMK knockdown boosted cardiomyocyte proliferation, dampened the markers of myocardial injury and inflammation, and injured apoptosis in the MI model, whereas GZMK overexpression aggravated cardiomyocyte MI injury. GZMK was positively mediated by WTAP in cardiomyocytes and was subjected to WTAP-mediated m⁶A modification. The low expression of GZMK reduced the MI area, attenuated myocardial tissue damage and inflammation, and arrested cardiomyocyte apoptosis in the MI rats. Thus, for the first time, we demonstrated that GZMK was modified by WTAP via m⁶A modification, which promoted its expression in MI, thereby aggravating MI-induced myocardial injury.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"463-471"},"PeriodicalIF":2.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144188663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"UBE2C, Regulated by n6-methyladenosine Methyltransferase METTL3, Is an Oncogene in Retinoblastoma via PI3K-AKT Pathway.","authors":"Lan Chen, Songhua Mei","doi":"10.1089/dna.2025.0074","DOIUrl":"10.1089/dna.2025.0074","url":null,"abstract":"<p><p>Retinoblastoma (RB) arising from the retina's primitive neural precursor cells is a highly aggressive pediatric ocular malignancy. Ubiquitin-conjugating enzyme E2C (UBE2C) is implicated in carcinogenesis, but its role and mechanism in RB remain unexplored. Here, we aimed to explore the effect of UBE2C and its regulatory mechanism in an N6-methyladenosine (m⁶A) modification method in RB. The expression of UBE2C and methyltransferase-like 3 (METTL3) was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting. After using shRNA and overexpression vectors to modulate the expression of UBE2C and METTL3 in RB cells, cell viability, proliferation, apoptosis, and phosphoinositide 3-kinase-protein kinase B (PI3K-AKT) pathway activity were assessed via cell counting kit-8, 5-ethynyl-2'-deoxyuridine, flow cytometry, and Western blotting assays, respectively. The correlation between METTL3 and UBE2C in RB cells was verified by qRT-PCR, Western blotting, methylated RNA immunoprecipitation, mRNA stability assays. The results showed that UBE2C with high expression in RB enhanced RB cell survival via elevating cell viability and proliferation, as well as suppressing apoptosis. UBE2C activated the PI3K-AKT pathway by promoting the PI3K and AKT proteins. METTL3 upregulated UBE2C expression and enhanced UBE2C mRNA stability via m⁶A modification. In addition, upregulating METTL3 partly restored the negative effects of UBE2C downregulation on RB cells. In conclusion, METTL3 drives UBE2C overexpression through m⁶A modification, thereby activating the PI3K-AKT pathway to foster RB progression. This study identifies the METTL3/UBE2C/PI3K-AKT axis as a novel therapeutic target for RB.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"436-444"},"PeriodicalIF":2.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ovine <i>TUSC5</i> and <i>IGFBP3</i> Gene Polymorphisms and their Association with Tail Fat Weight in Sheep.","authors":"Peiliang Cao, Deyin Zhang, Dan Xu, Zongwu Ma, Lijuan He, Mengru Pu, Guoxing Jia, Dewen Kong, Linting Li, Jian Zhang, Hongjian Li, Weiwei Wu, Fadi Li, Huibin Tian, Weimin Wang, Xiaoxue Zhang","doi":"10.1177/10445498251361047","DOIUrl":"10.1177/10445498251361047","url":null,"abstract":"<p><p>Tail fat weight is a key economic trait in fat-tailed sheep; reducing tail fat deposition is of significant importance for improving the economic efficiency of sheep farming. In this article, we measured the live weight before slaughter, tail fat weight, and carcass weight of Hu male sheep at 6 months of age and performed the descriptive statistical analysis. The results indicated the coefficient of variation of tail fat-related-traits ranged from 25% to 50%. Simultaneously, we selected <i>IGFBP3</i> and <i>TUSC5</i> as candidate genes based on their close association with fat deposition. Target regions were amplified using gene-specific primers in PCR, followed by Sanger sequencing of PCR products to identify genetic variants. Polymorphisms were subsequently validated using the KASPar genotyping assay. Finally, quantitative reverse transcription PCR (qRT-PCR) was performed to determine the expression levels of <i>IGFBP3</i> and <i>TUSC5</i>. Our findings revealed a missense mutation (g.83695349 C>T) in exon 1 of the <i>IGFBP3</i> gene and a synonymous mutation (g.41771645 C>T) in exon 2 of the <i>TUSC5</i> gene. Association analysis showed that these mutations were significantly correlated (<i>p</i> < 0.05) with tail fat weight traits. Moreover, the tail fat weight of the mutant genotypes (CT and TT) was significantly reduced compared with that of the CC genotype, suggesting that the gene may exert a negative regulatory effect on this trait, thereby leading to the reduction of tail fat weight. Furthermore, the genotype combinations showed a significant relationship with tail fat traits. Moreover, qRT-PCR results showed that <i>TUSC5</i> and <i>IGFBP3</i> genes were expressed in all experimental tissues of Hu sheep, and the highest expression was observed in tail fat compared with other tissues (heart, liver, spleen, lung, kidney, rumen, duodenum, muscle, and lymph). Notably, their expression levels were significantly lower in the large-tail fat group than in the small-tail fat group. Overall, these results will provide novel candidate variation for reducing tail fat deposition in sheep breeding practice.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"411-420"},"PeriodicalIF":2.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144710378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fertilization Initiates Seed Nutrition via Phloem End by a Callose Degradation Enzyme.","authors":"Ryushiro D Kasahara","doi":"10.1089/dna.2025.0106","DOIUrl":"10.1089/dna.2025.0106","url":null,"abstract":"<p><p>Why plants need fertilization to produce seeds has long been discussed. We recently identified a new specialized tissue required for seed formation at the ovule's chalazal end, showing the final form of the phloem end and supporting its transport function; however, it is blocked by callose deposition. Callose is removed after central cell fertilization (open state), allowing nutrients to be transported to the seed. However, if fertilization fails, callose deposition persists (closed state), preventing the tissue from transporting nutrients. A β-1,3-glucanase gene, AtBG_ppap, was identified, and the AtBG_ppap mutant showed the closed state, producing smaller seeds due to incomplete callose degradation. Contrarily, the AtBG_ppap overexpression line produced larger seeds due to continuous callose degradation, showing that the tissue is the \"gateway\" for the seed nutrients.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"407-410"},"PeriodicalIF":2.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144188662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autophagy and Reactive Oxygen Species in Megakaryopoiesis and Platelet Production.","authors":"Abbas Khosravi, Abtin Ghasempour, Mostafa Paridar, Pargol Mashati, Mina Darvishi, Mehraneh Karimzadeh, Rashin Mohseni, Amir Ali Hamidieh","doi":"10.1177/10445498251361641","DOIUrl":"https://doi.org/10.1177/10445498251361641","url":null,"abstract":"<p><p>Megakaryocytes (MKs), which are differentiated from megakaryocytic-erythrocytic progenitors, generate platelets (PLTs) by expanding and branching their cellular fragments under the influence of cytokines and intercellular mechanisms such as autophagy and release of reactive oxygen species (ROS) in the bone marrow. Autophagy is a self-destructive process that plays a significant role in cell growth and energy maintenance of the cells. In contrast, ROS are toxic products of cellular metabolism that are harmful to human stem cells but have a crucial role in determining lineage commitment at the common myeloid progenitor stage and deriving further maturation progression toward MKs and PLTs production, with an interconnected relationship in the onset and deriving of autophagy. This review summarizes and discusses what has been discovered about the current state of knowledge regarding autophagy effects on MK differentiation, ROS effects on megakaryopoiesis (MKp), and the relationship between these molecules and autophagy initiation. Furthermore, <i>in vitro</i> applications of controlling these external factors on MKp are reviewed according to pertinent studies. Utilizing these regulatory mechanisms supports an improved design of <i>in vitro</i> MKp for introducing artificial PLT sources and might be beneficial in creating novel treatments of PLT-related coagulation disorders.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144850086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>STING</i> rs7380824 Polymorphism Contributes to the Susceptibility of Colorectal Cancer in Chinese Population.","authors":"Xiufeng Zhang, WenLong Wu, Hongyan Li, Ying Jian, Ang Li, Zhi Zhang, Xuemei Zhang","doi":"10.1089/dna.2025.0020","DOIUrl":"10.1089/dna.2025.0020","url":null,"abstract":"<p><p><i>STING</i>, an endoplasmic reticulum-localized protein with multiple transmembrane domains, has been implicated in colorectal cancer (CRC) development. This study investigated the association between <i>STING</i> rs7380824 polymorphism and CRC susceptibility using both bioinformatics analysis and a case-control study. Bioinformatics predictions from SIFT and PolyPhen indicated that the rs7380824 variant, which results in an amino acid substitution from arginine (R) to glutamine (Q) at position 293, is likely to be deleterious, with a SIFT score of 0.000 and a PolyPhen score of 0.999. A total of 870 CRC patients and 870 healthy controls were genotyped using polymerase chain reaction-restriction fragment length polymorphism. Logistic regression analysis demonstrated that individuals carrying the CT and TT genotypes had an increased risk of CRC with OR (95% CI) of 1.564 (1.115-2.192) and 1.551 (1.271-1.893), respectively. Stratified analysis showed that the rs7380824 C > T variant increased CRC risk in all age and gender groups. Furthermore, non-smokers with the CT or TT genotype had a higher CRC risk (OR = 1.661, 95% CI: 1.333-2.071, <i>p</i> < 0.001), while no significant association was observed among smokers (<i>p</i> = 0.238). Similarly, non-drinkers carrying the CT or TT genotype showed an increased CRC risk (OR = 1.746, 95% CI: 1.395-2.185, <i>p</i> < 0.001), whereas no significant difference was detected among drinkers (<i>p</i> = 0.265). This study identifies <i>STING</i> rs7380824 polymorphism as a significant contributor to CRC susceptibility, with bioinformatics predictions and case-control analysis confirming its deleterious impact and the association with increased CRC risk. In addition, these findings underscore the interplay between genetic and environmental factors in CRC development, highlighting <i>STING</i>'s potential as a genetic biomarker for CRC risk assessment in the Chinese population.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"380-388"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144050373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of ETS2 in Macrophage Inflammation.","authors":"Christina T Stankey, James Christopher Lee","doi":"10.1089/dna.2025.0064","DOIUrl":"10.1089/dna.2025.0064","url":null,"abstract":"<p><p>Autoimmune and inflammatory diseases are rising globally yet widely effective therapies remain elusive. Most treatments have limited efficacy, significant potential side effects, or eventually lose response, underscoring the urgent need for new therapeutic approaches. We recently discovered that ETS2, a transcription factor, functions as a master regulator of macrophage-driven inflammation-and is causally linked to the pathogenesis of multiple inflammatory diseases via human genetics. The pleotropic inflammatory effects of ETS2 included upregulation of many cytokines that are individually targeted by current disease therapies, including TNFα, IL-23, IL1β, and TNF-like ligand 1A signaling. With the move toward combination treatment-to maximize efficacy-targeting ETS2 presents a unique opportunity to potentially induce a broad therapeutic effect. However, there will be multiple challenges to overcome since direct ETS2 inhibition is unlikely to be feasible. Here, we discuss these challenges and other unanswered questions about the central role that ETS2 plays in macrophage inflammation.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"339-344"},"PeriodicalIF":2.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7618055/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Active Ingredients of Herbs Targeting Long Noncoding RNA: A Potential Alternative to Treat Parenchymal Organ Inflammation and Fibrosis in the Future.","authors":"Min Zhou, Biyu Tan, Jian Liu, Qiong Zhang, Li Wang, Qiongdan Hu","doi":"10.1089/dna.2025.0058","DOIUrl":"10.1089/dna.2025.0058","url":null,"abstract":"<p><p>We review current studies on the anti-inflammatory and antifibrotic effects of herbal medicines and their active ingredients. To explore how these active ingredients target long noncoding RNA to exert their effects, we searched PubMed and Chinese National Knowledge Infrastructure databases for preclinical and clinical studies of long noncoding RNAs (lncRNA), herbal medicine, inflammation, and fibrosis. The active ingredients of herbal medicines were able to target lncRNAs. These interactions can have anti-inflammatory and antifibrotic effects on various diseases. The current studies provide preliminary insights but are not comprehensive. Targeting lncRNAs with herbal medicine ingredients is a promising direction for further research. This approach could lead to new alternative treatments for inflammation and fibrosis-related diseases.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"345-359"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144183207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of Cuproptosis Pathway Genes (DLAT, FDX1) and Antioxidant Enzyme Activities in Obese Mice in Response to Quercetin and Calorie Restriction.","authors":"Nima Mahdei Nasirmahalleh, Mina Hemmati, Negin Parsamanesh, Mohammad Borji","doi":"10.1089/dna.2025.0005","DOIUrl":"10.1089/dna.2025.0005","url":null,"abstract":"<p><p>Cuproptosis is a new mode of cell death that is closely related to mitochondrial stress. The purpose of this study is to investigate the amount of copper, copper-associated genes DLAT and FDX1 oxidative stress (OS) status in obesity. Since there is a close relationship between OS and cuproptosis, evaluating the effect of various strategies to reduce OS, including quercetin (QUER) and caloric restriction (CR), is another goal of this study. In this study, 30 male BALB-C mice aged 8 weeks and weighing 25 g, including the groups receiving normal diet (ND), ND with QUER (15 mg/kg, IP) and CR, a high-fat diet (HFD) with the QUER, CR or a combination of both were used. The activities of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPX), and glutathione reductase (GR), amount of copper in the liver and kidney tissues, and expression of DLAT and FDX1 genes were measured in all studied groups. The amount of copper in the liver and kidney tissue as well as the expression of FDX1 and DLAT in the HFD group increased significantly compared with the ND group. QUER, CR or their combination could significantly reduce the amount of copper as well as the expression of FDX1 and DLAT in liver and kidney tissues. QUER and CR, also significantly increased the activity of GR, SOD and GPX in serum, liver, and kidney tissues. Based on the results, QUER, CR and especially the simultaneous use of both, was able to reduce the amount of copper and its related cuproptosis. These effects may reduce cuproptosis-associated cell death. Therefore, the use of antioxidants and CR may be a promising solution to protect the human body against the effects of cuproptosis in conditions like obesity.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"370-379"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144033026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}