Epigenomics最新文献_第4页

Epigenetic investigation into NR3C1 exon 1F and HSD11B2: associations with neurodevelopment and oral feeding skills in preterm infants. NR3C1外显子1F和HSD11B2与早产儿神经发育和口腔喂养技能相关的表观遗传学研究

IF 2.6 4区医学

Epigenomics Pub Date : 2026-02-01 Epub Date: 2026-01-31 DOI: 10.1080/17501911.2026.2621199

Thao Griffith, George E Chlipala, Ashley Ford, Stefan J Green, Rosemary White-Traut, Sachin Amin, Lindsey Young, Caitlin Carlson, Linda Janusek

{"title":"Epigenetic investigation into NR3C1 exon 1F and HSD11B2: associations with neurodevelopment and oral feeding skills in preterm infants.","authors":"Thao Griffith, George E Chlipala, Ashley Ford, Stefan J Green, Rosemary White-Traut, Sachin Amin, Lindsey Young, Caitlin Carlson, Linda Janusek","doi":"10.1080/17501911.2026.2621199","DOIUrl":"10.1080/17501911.2026.2621199","url":null,"abstract":"Aims: To examine the relationship between DNA methylation of NR3C1 exon 1F and HSD11B2 promoters and neurodevelopment, and oral feeding skills in preterm infants.Design: A longitudinal prospective cohort study was conducted.Methods: Data from 61 preterm infants who were born between 26 to 34 weeks gestational age without major comorbidities were analyzed. DNA methylation was evaluated from buccal samples. Neurodevelopment and oral feeding skills were evaluated using the Neurobehavioral Assessment of the Preterm Infants and the Early Feeding Skills Assessment, respectively.Results: Increased methylation at specific cytosine-guanine (CpG) dinucleotide sites within NR3C1 exon 1F and HSD11B2 promoters was associated with suboptimal neurodevelopmental and oral feeding outcomes, potentially reflecting heightened sensitivity to early life stress in the NICU. Conversely, certain methylation changes appear to be adaptive, promoting consistent suck-breathe coordination, or optimal behavioral and cardiorespiratory stability during oral feeding.Conclusion: The study highlights the complex relationship between DNA methylation of NR3C1 exon 1F and HSD11B2 promoters and neurodevelopment, and oral feeding skills in preterm infants.Implications for the profession and/or patient care: Findings emphasize the need for continued research into epigenetic mechanisms underlying neonatal adaptation and stress regulation, with potential implications for targeted epigenetic interventions to support optimal neurodevelopment and oral feeding skills.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"185-196"},"PeriodicalIF":2.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12937114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146092373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

E2F1-driven cholesterol synthesis via the SND1/ACLY axis potentiates malignant progression in prostate cancer. 通过SND1/ACLY轴e2f1驱动的胆固醇合成增强前列腺癌的恶性进展。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-02-01 Epub Date: 2026-01-26 DOI: 10.1080/17501911.2026.2617186

Xiaopeng Zheng, Chengru Yang, Deqiang Bian, Guoxin Shi, Li Wang, Xiaohan Li, Yufei Chen, Hua Xin, Liming Wang

{"title":"E2F1-driven cholesterol synthesis via the SND1/ACLY axis potentiates malignant progression in prostate cancer.","authors":"Xiaopeng Zheng, Chengru Yang, Deqiang Bian, Guoxin Shi, Li Wang, Xiaohan Li, Yufei Chen, Hua Xin, Liming Wang","doi":"10.1080/17501911.2026.2617186","DOIUrl":"10.1080/17501911.2026.2617186","url":null,"abstract":"Aim: This study aimed to clarify the mechanisms of E2F transcription factor 1 (E2F1) in the Cholesterol (CHOL) synthesis of Prostate cancer (PCa).Methods: CHOL component content was detected using a commercial test kit. The interaction between E2F1 and staphylococcal nuclease domain-containing protein 1 (SND1) promoter was confirmed employing dual luciferase and chromatin immunoprecipitation assay. RNA immunoprecipitation and RNA pull-down analysis were utilized to validate the interaction between SND1 and ATP citrate lyase (ACLY) mRNA. A xenograft tumor model was used to confirm these mechanisms in vivo.Results: E2F1, SND1, ACLY protein levels, along with CHOL concentrations, were up-regulated in human PCa tumor tissues. E2F1 enhanced cell proliferation, invasion, and CHOL synthesis in PCa cells. E2F1 could transcriptionally activate SND1, which subsequently bound to ACLY mRNA, stabilizing its expression. E2F1 induced CHOL synthesis via the enhancement of SND1/ACLY axis. E2F1 promoted CHOL synthesis and PCa tumor growth in vivo.Conclusion: E2F1 enhanced cell proliferation, invasion, and tumor growth by enhancing CHOL synthesis via the SND1/ACLY axis in PCa models.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"155-168"},"PeriodicalIF":2.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12962671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146050768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of long non-coding RNA in the pathogenesis of aneurysms. 长链非编码RNA在动脉瘤发病机制中的作用。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-02-01 Epub Date: 2026-02-03 DOI: 10.1080/17501911.2026.2623931

Paulina Plewa, Maciej Ćmil, Anna Jędrasiak, Jan Zadworny, Andrzej Pawlik

{"title":"The role of long non-coding RNA in the pathogenesis of aneurysms.","authors":"Paulina Plewa, Maciej Ćmil, Anna Jędrasiak, Jan Zadworny, Andrzej Pawlik","doi":"10.1080/17501911.2026.2623931","DOIUrl":"10.1080/17501911.2026.2623931","url":null,"abstract":"Aneurysms are serious vascular conditions characterized by persistent dilatation of the blood vessel lumen, which can lead to rupture and become life-threatening. Their pathogenesis is complex and involves multiple biological mechanisms, including extracellular matrix degradation, oxidative stress, inflammation, and apoptosis of vascular smooth muscle cells. Long non-coding RNAs (lncRNAs), typically exceeding 200 nucleotides, perform numerous regulatory functions, including modulation of gene expression at the epigenetic, transcriptional, and post-transcriptional levels. Under pathological conditions, lncRNA expression can be markedly altered. A growing body of evidence indicates that lncRNAs play a key role in regulating cellular processes such as inflammation, apoptosis, and vascular remodeling, all of which are crucial to aneurysm development and progression. This review summarizes current knowledge on the involvement of lncRNAs in aneurysm pathophysiology and highlights recent research on their impact on vascular wall degradation, inflammatory responses, and smooth muscle cell survival. A literature review was conducted through a systematic search of PubMed, Scopus, and Web of Science using keywords related to lncRNAs and biological processes relevant to aneurysm development.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"231-242"},"PeriodicalIF":2.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12962698/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146112666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Interaction of host genetic factor and gastric microbiome in DNA methylation induction. 宿主遗传因子与胃微生物组在DNA甲基化诱导中的相互作用。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-02-01 Epub Date: 2026-02-09 DOI: 10.1080/17501911.2026.2627274

Tomomitsu Tahara, Tsubasa Shimogama, Takuya Shijimaya, Jumpei Yamazaki, Naohiro Nakamura, Yu Takahashi, Makoto Naganuma

引用次数: 0

MicroRNAs in esophageal squamous cell carcinoma. 食管鳞状细胞癌中的microrna。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-02-01 DOI: 10.1080/17501911.2026.2624361

Qi-Wei Liu, Zi-Qin Liu, Ming Wang, Yi-Jun Qi

引用次数: 0

Mitochondrial D-loop region methylation differentiates Parkinson's disease from atypical parkinsonism and Parkinson's disease dementia. 线粒体d环区甲基化可区分帕金森病与非典型帕金森病和帕金森病痴呆。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-02-01 Epub Date: 2026-02-11 DOI: 10.1080/17501911.2026.2627263

Bilge Karacicek, Bilgesu Ozturk, Ozgur Oztop Cakmak, Fatos Sibel Ertan, Pembe Keskinoglu, Sermin Genc

{"title":"Mitochondrial D-loop region methylation differentiates Parkinson's disease from atypical parkinsonism and Parkinson's disease dementia.","authors":"Bilge Karacicek, Bilgesu Ozturk, Ozgur Oztop Cakmak, Fatos Sibel Ertan, Pembe Keskinoglu, Sermin Genc","doi":"10.1080/17501911.2026.2627263","DOIUrl":"10.1080/17501911.2026.2627263","url":null,"abstract":"Background: Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by dopaminergic neuron loss and α-synuclein aggregation. Epigenetic mechanisms, including mitochondrial DNA (mtDNA) methylation, have been implicated in PD pathogenesis. Methylation of the mitochondrial displacement loop (D-loop) region may play a role in neurodegenerative processes.Research design and methods: This case study assessed D-loop methylation levels in peripheral blood samples from 37 patients with PD, 18 patients with Parkinson's disease dementia (PD-D), 26 patients with atypical parkinsonism (APS), and 26 healthy controls (HC). Associations with clinical parameters, sex, and L-dopa treatment were analyzed.Results: D-loop methylation levels were significantly reduced in patients with PD-D and APS compared to PD patients and HC. Methylation levels were not associated with disease duration, clinical variables, sex, or L-dopa treatment.Conclusions: Decreased mitochondrial D-loop methylation in PD-D and APS may reflect disease-specific epigenetic mechanisms rather than clinical characteristics or treatment effects.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"197-204"},"PeriodicalIF":2.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12962608/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146156431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Methylation changes of gallbladder DNA during the formation of gallstones. 胆结石形成过程中胆囊DNA的甲基化变化。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-01-01 Epub Date: 2026-01-07 DOI: 10.1080/17501911.2025.2610614

Hongyu Xu, Jinlong Hu, Jinshan Liu, Rui Wang, Junbin Peng, Peilin Liu, Jiaming Yao, Baoqiang Cao

{"title":"Methylation changes of gallbladder DNA during the formation of gallstones.","authors":"Hongyu Xu, Jinlong Hu, Jinshan Liu, Rui Wang, Junbin Peng, Peilin Liu, Jiaming Yao, Baoqiang Cao","doi":"10.1080/17501911.2025.2610614","DOIUrl":"10.1080/17501911.2025.2610614","url":null,"abstract":"Objective: To investigate the genome-wide methylation changes in gallbladder tissues during gallstone formation, as well as alterations in key signaling pathways and associated gene expression.Methods: A combined methylation and transcriptomic analysis was performed on gallbladder tissues from gallstone model mice and normal control mice using reduced representation bisulfite sequencing (RRBS) and RNA high-throughput sequencing. Key candidate genes were validated using qRT-PCR, Western blotting, and immunohistochemistry. Cross-species validation was conducted using human gallbladder transcriptomic data from GEO datasets.Results: Integrated RRBS and RNA-seq analysis revealed that abnormal DNA methylation may contribute to gallstone formation by dysregulating gene expression in pathways associated with gallbladder dysfunction. A total of 97 differentially methylated and expressed genes exhibiting significant inverse correlations between methylation and expression levels were identified. The top six genes with the strongest correlations were experimentally validated. Analysis of human gallstone samples identified partial overlapping differentially expressed genes with the mouse model.Conclusion: This study demonstrates the potential roles of DNA methylation and gene expression changes in gallbladder tissue during the formation of gallstones. These findings provide a new perspective for further understanding the causes of gallstones and searching for possible clinical therapies.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"55-71"},"PeriodicalIF":2.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12826745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145910793","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genome-wide methylation patterns associated with chronic stress. 与慢性应激相关的全基因组甲基化模式。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-01-01 Epub Date: 2026-01-09 DOI: 10.1080/17501911.2026.2613012

Nicholas O'Toole, Tie-Yuan Zhang, Eamon Fitzgerald, Xianglan Wen, Josie Diorio, Patricia P Silveira, Benoit Labonté, Eric J Nestler, Michael J Meaney

{"title":"Genome-wide methylation patterns associated with chronic stress.","authors":"Nicholas O'Toole, Tie-Yuan Zhang, Eamon Fitzgerald, Xianglan Wen, Josie Diorio, Patricia P Silveira, Benoit Labonté, Eric J Nestler, Michael J Meaney","doi":"10.1080/17501911.2026.2613012","DOIUrl":"10.1080/17501911.2026.2613012","url":null,"abstract":"Background: Chronic social defeat stress (CSDS) is a validated animal model for depression that produces sustained behavioral and transcriptional changes in the brain, notably the nucleus accumbens (nAcc).Research design and methods: We used genome-wide analysis of cytosine methylation patterns in mouse nAcc following CSDS to identify candidate epigenetic mechanisms.Results: CSDS produced extensive differential methylation, increasing CG hypermethylation compared to control conditions; non-CG methylation showed the opposite trend. Highly differentially methylated (DM) regions included several genes implicated in behavioral effects of CSDS, including estrogen receptor alpha (Esr1).Conclusions: Analysis of DM sites within gene bodies revealed ß-catenin as a hub gene of a network including the ß-catenin-related WNT/frizzled signaling pathway. Analysis of DM sites upstream of transcription start sites revealed a gene network with the Tcf4 transcription factor as a hub. Genes DM within the gene body were enriched for synaptic function and primarily expressed in D1+ and D2+ medium spiny neurons, which, like the WNT/ß-catenin pathway, are estrogen sensitive and implicated in the behavioral effects of CSDS. We found significant overlap between DM genes associated with CSDS and those associated with major depressive disorder in genome-wide association studies, suggesting that effects on DNA methylation are implicated in the molecular pathways that link chronic stress to depression.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"73-88"},"PeriodicalIF":2.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12863070/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145932735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mitochondrial DNA copy number reduction via in vitro TFAM knockout remodels the nuclear epigenome and transcriptome. 通过体外敲除TFAM减少线粒体DNA拷贝数重塑核表观基因组和转录组。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-01-01 Epub Date: 2025-12-23 DOI: 10.1080/17501911.2025.2603883

Phyo W Win, Julia Nguyen, Elly H Shin, Tyler S Nagano, Brent Selimi, Katie Hong, Anahita M Meybodi, Bradley P Yates, Emma V Burke, David E Carter, Gregory A Newby, Charles Newcomb, Dan E Arking, Christina A Castellani

{"title":"Mitochondrial DNA copy number reduction via in vitro TFAM knockout remodels the nuclear epigenome and transcriptome.","authors":"Phyo W Win, Julia Nguyen, Elly H Shin, Tyler S Nagano, Brent Selimi, Katie Hong, Anahita M Meybodi, Bradley P Yates, Emma V Burke, David E Carter, Gregory A Newby, Charles Newcomb, Dan E Arking, Christina A Castellani","doi":"10.1080/17501911.2025.2603883","DOIUrl":"10.1080/17501911.2025.2603883","url":null,"abstract":"Aims: Mitochondrial DNA copy number (mtDNA-CN) is associated with several age-related chronic diseases and is a predictor of all-cause mortality. Here, we examine site-specific differential nuclear DNA (nDNA) methylation and differential gene expression resulting from in vitro reduction of mtDNA-CN to uncover shared genes and biological pathways mediating the effect of mtDNA-CN on disease.Materials and methods: Epigenome and transcriptome profiles were generated for three independent human embryonic kidney (HEK293T) cell lines harboring a mitochondrial transcription factor A (TFAM) knockout generated via CRISPR-Cas9, and matched control lines.Results: We identified 2924 differentially methylated sites, 67 differentially methylated regions, and 102 differentially expressed genes associated with mtDNA-CN. Integrated analysis uncovered 24 Gene-CpG pairs. GABAA receptor genes and related pathways, the neuroactive ligand signaling pathway, ABCD1/2 gene activity, and cell signaling processes were overrepresented, providing insight into the underlying biological mechanisms facilitating these associations. We also report evidence implicating chromatin state regulatory mechanisms as modulators of mtDNA-CN effect on gene expression.Conclusions: We demonstrate that mitochondrial DNA variation signals to the nuclear DNA epigenome and transcriptome and may lead to nuclear remodeling relevant to development, aging, and complex disease.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"27-44"},"PeriodicalIF":2.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12826749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145810078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

ALKBH5-mediated m6A demethylation of TXNDC5 drives malignant progression in gastric cancer. alkbh5介导的TXNDC5 m6A去甲基化驱动胃癌恶性进展。

IF 2.6 4区医学

Epigenomics Pub Date : 2026-01-01 Epub Date: 2025-11-11 DOI: 10.1080/17501911.2025.2586450

Wenkun Peng, Xiaoquan Wei, Feifei Zhou, Hongwei Xu

{"title":"ALKBH5-mediated m6A demethylation of TXNDC5 drives malignant progression in gastric cancer.","authors":"Wenkun Peng, Xiaoquan Wei, Feifei Zhou, Hongwei Xu","doi":"10.1080/17501911.2025.2586450","DOIUrl":"10.1080/17501911.2025.2586450","url":null,"abstract":"Background: Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide. N6-methyladenosine (m6A) modification plays a critical role in post-transcriptional gene regulation. This study aimed to elucidate the molecular mechanism by which the RNA demethylase ALKBH5 regulates GC progression through m6A modification of thioredoxin domain-containing protein 5 (TXNDC5).Methods: Differential expression models of ALKBH5 and TXNDC5 were established in GC cells using RNA interference and gene overexpression. Methylated RNA immunoprecipitation (MeRIP-qPCR), qPCR, and Western blot were performed to assess ALKBH5-mediated m6A modification and its effect on TXNDC5 expression. Functional assays, including proliferation, migration, and invasion, as well as a xenograft mouse model, were used to evaluate their roles in GC progression.Results: ALKBH5 was significantly upregulated in GC tissues and cells. Overexpression of ALKBH5 stabilized TXNDC5 expression in an m6A-dependent manner, thereby promoting malignant phenotypes. Conversely, ALKBH5 knockdown increased m6A methylation of TXNDC5, reduced TXNDC5 protein expression, and suppressed GC cell proliferation, migration, and invasion. In vivo experiments confirmed that loss of ALKBH5 impaired tumor growth.Conclusions: Our findings demonstrate that the ALKBH5-TXNDC5 axis drives GC progression through m6A-dependent regulation, highlighting ALKBH5 as a potential therapeutic target for GC.","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"15-26"},"PeriodicalIF":2.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12826721/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145488193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0