{"title":"Nucleosome Linker Length and Distribution as Major Players in Epigenetic Regulation: Insights from Cryo-Electron Microscopy and Modeling of Retina Cell Maturation.","authors":"Tamar Schlick, Sergei Grigoryev","doi":"10.1177/10445498251381313","DOIUrl":"https://doi.org/10.1177/10445498251381313","url":null,"abstract":"<p><p>We summarize recent findings on the conformational differences of chromatin fibers in immature versus mature retina cells due to different nucleosome linker length values and distributions, as revealed by cryo-electron microscopy and modeling studies, emphasizing implications to chromatin organization and epigenetic regulation broadly.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145188110","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":"m6A Modification Destabilizes Prss8 and Activates Hepatic Stellate Cells via TLR4-Mediated Inflammatory Responses.","authors":"Huimei Chen, Linhui Zhang, Lili Zhang, Tao Liu, Xue Pang, Chang Fan, Hui Jiang","doi":"10.1177/10445498251380337","DOIUrl":"https://doi.org/10.1177/10445498251380337","url":null,"abstract":"<p><p>The 6-methyladenine (m6A) modification plays a major role in various diseases. Serine protease 8 (<i>Prss8</i>) contributes to the initiation and progression of liver fibrosis (LF). However, the mechanism by which the m6A modification of <i>Prss8</i> induces hepatic stellate cells (HSCs) activation in the LF is unclear. This study focused on exploring the contribution of <i>Prss8</i> m6A modification to the pathogenesis of LF. First, primary hepatic parenchymal cells (hepatocytes) and HSCs were isolated from a mouse model of LF, and a coculture of these two types of cells was used as the object of study. Then, real-time fluorescence quantitative PCR, methylated RNA immunoprecipitation, and Western blotting were used to test the expression levels of <i>Prss8</i> mRNA and protein, <i>Prss8</i> m6A modification, <i>Collagen I</i>, <i>α-SMA</i>, and <i>TLR4</i>. Finally, the expression levels of inflammatory markers were measured via an enzyme-linked immunosorbent assay. Compared with the control group, the model group presented significantly lower <i>Prss8</i> mRNA and protein levels in hepatocytes but greater levels of <i>Prss8</i> m6A modification; moreover, the expression of HSC activation markers and the <i>TLR4</i>, <i>IL-1β</i>, and <i>IL-18</i> proteins was significantly elevated. Mutation of the <i>Prss8</i> m6A modification site led to upregulation of <i>Prss8</i> mRNA and protein and decreased levels of m6A modification, <i>TLR4</i>, <i>IL-1β</i>, and <i>IL-18</i>. Furthermore, mutation of the <i>Prss8</i> m6A modification site increased the stability of <i>Prss8</i> mRNA. Rescue experiments confirmed the regulatory link between <i>Prss8</i> m6A modification and <i>TLR4</i>. Overall, <i>Prss8</i> m6A modification decreases the stability of its mRNA, promoting <i>TLR4</i>-mediated inflammatory cascades and leading to excessive activation of HSCs. Targeting <i>Prss8</i> m6A modification is a promising therapeutic strategy for LF.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145139818","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":"New Insights into Host Genetic Ancestry as a Risk Factor for Dengue Disease.","authors":"Simon M Barratt-Boyes, Priscila M S Castanha","doi":"10.1177/10445498251379003","DOIUrl":"https://doi.org/10.1177/10445498251379003","url":null,"abstract":"<p><p>Dengue is the most important mosquito-borne viral infection of humans worldwide. Genetic ancestry of the host is a significant risk factor for severe dengue, but the mechanisms are not known. Recent findings using human skin explants from genetically defined donors reveal that dengue virus (DENV) replication and spread in skin increases with increasing proportion of European ancestry of the donor, associated with a strong inflammatory response and local myeloid cell infiltration, infection, and migration. In contrast, African ancestry is associated with substantially reduced cutaneous inflammation and cell infiltration following virus inoculation, resulting in reduced infection and migration of infected cells. These findings help explain the long-standing observation that individuals of African descent are relatively protected against severe dengue, while individuals of European descent are not. In this essay, we review DENV infection, focusing on human skin and the influence of genetic ancestry on the cutaneous innate response and virus spread.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145115647","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":"KIAA1429 Induces the Tumorigenesis of Clear Cell Renal Cell Carcinoma via Regulating the <i>N</i><sup>6</sup>-Methyladenosine Modification of Thymosin Beta-10.","authors":"Sheng Jin, Fang Liu","doi":"10.1177/10445498251381257","DOIUrl":"https://doi.org/10.1177/10445498251381257","url":null,"abstract":"<p><p><i>N</i><sup>6</sup>-Methyladenosine (m<sup>6</sup>A) is a reversible RNA modification that regulates tumorigenesis. KIAA1429, a critical component of the m<sup>6</sup>A methyltransferase complex, has an unclear role in clear cell renal cell carcinoma (ccRCC). Here, we investigated the role of KIAA1429 in ccRCC tumorigenesis. The expressions of KIAA1429 and thymosin beta-10 (TMSB10) in ccRCC samples were evaluated using quantitative real-time PCR (qRT-PCR). The malignant features of ccRCC cells were assessed via CCK-8, colony formation, transwell migration, and invasion assays, as well as <i>in vivo</i> tumor xenograft models. The relationship between KIAA1429 and TMSB10 was verified via Pearson correlation analysis, methylated RNA immunoprecipitation, qRT-PCR, and Western blotting assays. Functional rescue experiments further confirmed their interaction. We found that KIAA1429 was highly expressed in ccRCC, and its silencing significantly suppressed cell proliferation, migration, invasion, and tumor growth <i>in vivo</i>, while overexpression had the opposite effect. Bioinformatics and mechanistic analyses identified TMSB10 as a downstream target of KIAA1429, whose expression was upregulated in an m<sup>6</sup>A-dependent manner. Furthermore, overexpressing TMSB10 partially reversed the inhibitory effects of KIAA1429 silencing on ccRCC cells. Moreover, TMSB10 overexpression partially reversed the inhibitory effects of KIAA1429 knockdown. Taken together, our findings demonstrate that KIAA1429 promotes ccRCC tumorigenesis by enhancing TMSB10 expression via m<sup>6</sup>A modification, suggesting it as a potential prognostic biomarker and therapeutic target. However, the lack of clinical validation limits the immediate translational impact of these findings.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145115696","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":"Polymorphism of BIK as a Host Risk Factor for Severe Influenza.","authors":"Sourabh Soni, Yohannes A Mebratu","doi":"10.1177/10445498251379681","DOIUrl":"https://doi.org/10.1177/10445498251379681","url":null,"abstract":"<p><p>This essay focuses on a key host factor, the protein BIK (Bcl-2-interacting killer), that influences the severity of influenza A virus (IAV) infections. Our recent research published in Proceedings of the National Academy of Sciences describes a novel IAV-BIK-β5 axis that is critical for viral replication. The study demonstrates that BIK is essential for efficient IAV replication, and its overexpression leads to increased viral loads, lung inflammation, and heightened mortality in mouse models. We also identified a single nucleotide polymorphism (SNP), rs738276, in the BIK gene's promoter. This SNP influences the basal expression of BIK, and individuals with the high-expression AA genotype are at a higher risk for severe influenza. The molecular mechanism involves the viral nucleoprotein (NP) suppressing the proteasome's β5 subunit, which leads to BIK accumulation and promotes viral replication. These findings identify BIK as a potential therapeutic target and the rs738276 SNP as a biomarker for personalized medicine.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145093246","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>Retraction:</i> Melatonin Inhibits the Proliferation of Gastric Cancer Cells Through Regulating the miR-16-5p-Smad3 Pathway.","authors":"","doi":"10.1177/10445498251371637","DOIUrl":"10.1177/10445498251371637","url":null,"abstract":"","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145076880","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":"Probiotic Feed Additive from Indigenous <i>Bacillus subtilis</i> Enhances Growth and Health in Common Carp (<i>Cyprinus carpio</i>).","authors":"Havan Dwud Sleman, Nasreen Mohialddin Abdulrahman","doi":"10.1177/10445498251370558","DOIUrl":"https://doi.org/10.1177/10445498251370558","url":null,"abstract":"<p><p>Probiotics sourced from host-adapted microbes represent a sustainable innovation in aquaculture nutrition, aiming to replace antibiotics and enhance fish health. However, studies evaluating indigenous probiotic strains specifically adapted to the gut environment of target species remain limited. In this study, an indigenous <i>Bacillus subtilis</i> strain was isolated from common carp (<i>Cyprinus carpio</i>) intestine, PCR-authenticated via dual endoglucanase amplicons (545 and 1311 bp), formulated as a powdered feed additive, and tested at 1, 10, and 100 mg/kg against commercial Nutri-Fish®, Infloran Bio®, vitamin C, and a supplemented control in an 8-week feeding trial with (<i>n</i> = 126) carp. The 10 mg/kg dose significantly (<i>p</i> < 0.05) enhanced growth performance, producing the highest weight gain (133.27 ± 4.56 g), specific growth rate (2.59 ± 0.12% per day), and relative growth rate (43.09 ± 1.23%), along with improved feed conversion ratio (3.51 ± 0.09%), feed efficiency ratio (29.58 ± 1.45%), and protein efficiency ratio (475.95 ± 15.32%). Hematological analysis revealed neutrophilia (52%, <i>p</i> < 0.05), a moderated neutrophil-to-lymphocyte ratio, and stable erythron parameters, indicating primed innate immunity without systemic stress. Plasma alanine aminotransferase and aspartate aminotransferase levels decreased by 30-40% relative to other groups (<i>p</i> < 0.05), evidencing improved hepatic integrity and lipid metabolism. Intestinal histology showed moderate mucosal fold hypertrophy at 10 mg/kg, whereas the highest dose (100 mg/kg) caused epithelial sloughing and inflammation. These results demonstrate that a precision microdose (10 mg/kg) of host-adapted <i>B. subtilis</i> can outperform multicomponent commercial supplements by significantly enhancing growth, immunity, and organ health. This probiotic strategy provides a sustainable, eco-friendly alternative for warm-water carp aquaculture, supporting circular economy principles and reducing reliance on antibiotics.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144983858","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}
DNA and cell biologyPub Date : 2025-09-01Epub Date: 2025-07-14DOI: 10.1177/10445498251359374
Yuan Tian, Chen He
{"title":"Exosome-Mediated circRNA Hsa_Circ_0113050 Enhances Colorectal Cancer Cell Malignancy by Interacting with EIF4A3.","authors":"Yuan Tian, Chen He","doi":"10.1177/10445498251359374","DOIUrl":"10.1177/10445498251359374","url":null,"abstract":"<p><p>The exosome-mediated circular RNAs (circRNAs) play a crucial role in tumorigenesis. The present study investigated the role of the exosome-mediated circRNA hsa_circ_0113050 in colorectal cancer (CRC) through its interaction with the eukaryotic translation initiation factor 4A3 (EIF4A3). CRC-derived exosomes were isolated and characterized by differential ultracentrifugation, transmission electron microscopy, and nanoparticle tracking analysis. The hsa_circ_0113050 expressions in CRC and exosomes were confirmed through a bioinformatic analysis and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) assays. Cell functional and <i>in vivo</i> assays were applied to evaluate the effects of exosomes and hsa_circ_0113050 on CRC cell malignancy. The interaction between EIF4A3 and hsa_circ_0113050 was analyzed by RNA immunoprecipitation, Western blotting, and qRT-PCR assays. CRC-derived exosomes with diameters of 102 and 104 nm enhanced the ability of CRC cells to proliferate, migrate, and invade. hsa_circ_0113050 was highly expressed in CRC tissues and CRC-derived exosomes. Silencing hsa_circ_0113050 in exosomes effectively reversed the exosome-induced CRC cell malignancy. Furthermore, EIF4A3 bound to the linear gene (EIF3I) of hsa_circ_0113050 to enhance the hsa_circ_0113050 expression in the CRC cells. In conclusion, the present study is the first to reveal that exosome-mediated hsa_circ_0113050 enhances CRC cell malignancy by interacting with EIF4A3. Our study findings provide new mechanistic insights into circRNA regulation and highlight a potential therapeutic target for CRC.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"512-521"},"PeriodicalIF":2.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144628219","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}
DNA and cell biologyPub Date : 2025-09-01Epub Date: 2025-07-15DOI: 10.1177/10445498251359370
Guanyi He, Jie Qing
{"title":"Bile Acid-Mediated Interactions with Various Cell Types in the Cholestatic Liver.","authors":"Guanyi He, Jie Qing","doi":"10.1177/10445498251359370","DOIUrl":"10.1177/10445498251359370","url":null,"abstract":"<p><p>Bile acids (BAs) have garnered significant attention due to their novel roles in modulating diverse host physiological processes. They play a crucial role in nutrient transport, organelle function, and maintaining the systemic balance of pro/anti-inflammatory states. BAs exert complex physiological effects through their interaction with nuclear receptors, such as farnesoid X receptor or cell membrane receptor Takeda G protein-coupled receptor 5. Disruption of BA transport and homeostasis results in the accumulation of BAs and elevated concentrations in the systemic circulation. This contributes to the pathogenesis of cholestatic disorders and is implicated in a variety of liver diseases, including primary biliary cholangitis and primary sclerosing cholangitis. In the context of cholestatic liver injury, BAs interact with parenchymal hepatocytes and nonparenchymal cells, leading to hepatocyte apoptosis, activation of hepatic stellate cells, and the initiation of inflammatory responses. Identifying key cellular and molecular components involved in this interaction may contribute to the development of potential therapies for cholestatic liver diseases. In this article, we provide a summary of the molecular mechanisms underlying BA-mediated interactions with various cell types in the cholestatic liver and discuss therapeutic strategies targeting BA pathways. We anticipate that a deeper understanding of these interactions will enable the formulation of novel strategies for the treatment of cholestatic liver injury.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"502-511"},"PeriodicalIF":2.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144639018","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":"Genetic Underpinnings of Mitochondrial Cardiomyopathy: A Scoping 2010-2024 Update.","authors":"Insaf Moudian, Joaira Bakkach, Zeineb Zian, Naima Ghailani Nourouti, Amina Barakat, Mohcine Bennani Mechita","doi":"10.1089/dna.2025.0089","DOIUrl":"10.1089/dna.2025.0089","url":null,"abstract":"<p><p>Mitochondrial cardiomyopathy is a rare specific myocardial condition characterized by abnormal myocardium structure and/or function due to mitochondrial respiratory chain deficiency. This cardiac disorder results from mutations in mitochondrial DNA or nuclear genes affecting mitochondrial function. These mutations disrupt oxidative phosphorylation and consequently lead to energy deficit in the myocardial tissue and systemic symptoms due to impaired mitochondrial metabolism. In the current review, we aimed to highlight genetic and molecular underpinnings of mitochondrial cardiomyopathy. The impact of mitochondrial DNA characteristics on mitochondrial cardiomyopathy, mutations in both mitochondrial and nuclear genomes, as well as diagnostic limitations and future therapies, will be presented in this work.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"473-485"},"PeriodicalIF":2.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144546632","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}