Epigenetics最新文献

{"title":"ACMSD methylation in peripheral blood is associated with dynamic functional connectivity pattern in adolescent MDD patients.","authors":"Maojia Ran, Meijiang Jin, Zhujun Wang, Hang Zhang, Yuanmei Tao, Hanmei Xu, Shoukang Zou, Fang Deng, Hong Zhang, Xiaowei Tang, Xia Fu, Li Yin","doi":"10.1080/15592294.2025.2560339","DOIUrl":"10.1080/15592294.2025.2560339","url":null,"abstract":"<p><p>This study aimed to explore the association between ACMSD methylation level in peripheral blood and brain dynamic functional connectivity (dFC) patterns in adolescents with MDD. Sixty-seven drug-naive, first-episode adolescents with MDD (mean age 14.55 ± 1.38 years, 24 males [35.8%]) and twenty-three healthy controls (HCs, mean age 14.34 ± 1.47 years, 10 males [43.5%]) completed resting-state structural and functional magnetic resonance imaging. DNA samples were collected from peripheral venous blood. Joint and Individual Variation Explained (JIVE) method was used to explore the joint and independent components of four domains of environmental factors (life adverse events, LAE; family environment, FE; family functioning, FF; childhood chronic stress, CCS). Dynamic independent component analysis was used to compute dynamic functional connectivity between brain regions. Associations between ACMSD methylation, environment and brain dFC patterns were assessed. JIVE calculated one joint (JIVE-joint) and seven individual components (JIVE-LAE-1, JIVE-FE-1, JIVE-FE-2, JIVE-FF-1, JIVE-FF-2, JIVE-CCS-1, and JIVE-CCS-2). ACMSD methylation was negatively correlated with JIVE-joint (<i>r</i> = -0.304, <i>p</i> = 0.012) and JIVE-CCS-1 (<i>r</i> = -0.299, <i>p</i> = 0.014) but positively correlated with JIVE-CCS-2 (<i>r</i> = 0.248, <i>p</i> = 0.043). Greater ACMSD methylation was associated with increased dFC strength between the left lateral occipital cortex and right postcentral gyrus (PostCG; T[65] = 4.02, <i>p</i> < 0.001, <i>p</i>-FDR = 0.010) and between the left temporal occipital fusiform cortex and right PostCG (T[65] = 3.86, <i>p</i> < 0.001, <i>p</i>-FDR = 0.035) in adolescent MDD patients. Methylation value of the ACMSD gene is more likely to be influenced by childhood chronic stress. This study may provided a new perspective for future epigenetic research on adolescent MDD.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2560339"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12452479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TET-mediated 5hmC in breast cancer: mechanism and clinical potential.","authors":"Jiahang Zhang, Nadire Aishan, Zhongqiu Zheng, Siwei Ju, Qina He, Qingna Meng, Xixi Lin, Jiaheng Lang, Jichun Zhou, Yongxia Chen, Bojian Xie, Yangjun Cai, Feiyang Ji, Linbo Wang","doi":"10.1080/15592294.2025.2473250","DOIUrl":"10.1080/15592294.2025.2473250","url":null,"abstract":"<p><p>Breast cancer is the most common cancer among women, with differences in clinical features due to its distinct molecular subtypes. Current studies have demonstrated that epigenetic modifications play a crucial role in regulating the progression of breast cancer. Among these mechanisms, DNA demethylation and its reverse process have been studied extensively for their roles in activating or silencing cancer related gene expression. Specifically, Ten-Eleven Translocation (TET) enzymes are involved in the conversion process from 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), which results in a significant difference in the global level of 5hmC in breast cancer compared with normal tissues. In this review, we summarize the functions of TET proteins and the regulated 5hmC levels in the pathogenesis of breast cancer. Discussions on the clinical values of 5hmC in early diagnosis and the prediction of prognosis are also mentioned.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2473250"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11869774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143523066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering the interplay between SETD2 mediated H3K36me3 and RNA N6-methyladenosine in clear cell renal cell carcinoma (ccRCC).","authors":"Shafiq Shaikh, Xia Zhao, Ryan T Wagner, Xiaoyu Pan, Ryan A Hlady, Liguo Wang, Thai H Ho, Keith D Robertson","doi":"10.1080/15592294.2025.2456418","DOIUrl":"10.1080/15592294.2025.2456418","url":null,"abstract":"<p><p>RNA N6-methyladenosine (m6A) plays diverse roles in RNA metabolism and its deregulation contributes to tumor initiation and progression. Clear cell renal cell carcinoma (ccRCC) is characterized by near ubiquitous loss of <i>VHL</i> followed by mutations in epigenetic regulators <i>PBRM1</i>, <i>SETD2</i>, and <i>BAP1</i>. Mutations in <i>SETD2</i>, a histone H3 lysine 36 trimethylase (H3K36me3), are associated with reduced survival, greater metastatic propensity, and metabolic reprogramming. While m6A and H3K36me3 deregulation are separately implicated in renal tumorigenesis, H3K36me3 may participate directly in m6A targeting, but the m6A-H3K36me3 interplay has not been investigated in the context of ccRCC. Using RCC-relevant SETD2 isogenic knockout and rescue cell line models, we demonstrate a dynamic redistribution of m6A in the SETD2 depleted transcriptome, with a subset of transcripts involved in metabolic reprogramming demonstrating SETD2 dependent m6A and expression level changes. Using a panel of six histone modifications we show that m6A redistributes to regions enriched in gained active enhancers upon <i>SETD2</i> inactivation. Finally, we demonstrate a reversal of transcriptomic programs involved in SETD2 loss mediated metabolic reprogramming, and reduced cell viability through pharmacologic inhibition or genetic ablation of m6A writer METTL3 specific to SETD2 deficient cells. Thus, targeting m6A may represent a novel therapeutic vulnerability in <i>SETD2</i> mutant ccRCC.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2456418"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11776469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA methylation and bronchiectasis: a Mendelian randomization analysis to investigate causal link and therapeutic target.","authors":"Jiangyue Qin, Bi Ran, Lian Liu, Ping Li, Zhenni Chen, Diandian Li, Yongchun Shen, Fuqiang Wen","doi":"10.1080/15592294.2025.2521622","DOIUrl":"10.1080/15592294.2025.2521622","url":null,"abstract":"<p><p>This study aims to discover drug targeted genes and explore the potential epigenetics mechanisms in bronchiectasis. Cis-expression quantitative trait locus (eQTL) was obtained as exposure, and bronchiectasis from the FinnGen cohort was used as outcome. Mendelian Randomization (MR) was performed to identify therapeutic targets associated with bronchiectasis. Colocalization and summary-data-based MR (SMR) analyses were carried out to further confirm the causal roles of candidate genes in bronchiectasis. The value of these drug targets was validated via drug prediction and molecular docking. Finally, we used mediation analysis to identify the DNA methylation QTLs to bronchiectasis mediated by candidate genes. Ten drug targets were significantly associated with bronchiectasis. Strong evidence for the colocalization of <i>ACVR2A</i> and <i>VRK2</i> with bronchiectasis was found (PP.H4 > 0.75). SMR analysis revealed that higher expressions of <i>DDR1</i> and <i>VRK2</i> were linked to a higher risk of bronchiectasis, and higher expressions of <i>SCD5</i>, <i>TNFRSF4</i> and <i>XCL2</i> were linked to a lower risk of bronchiectasis. Finally, mediation analysis revealed potential causality effect of the DNA methylation site cg21568453 to bronchiectasis risk via <i>VRK2</i>. The increased expression of <i>VRK2</i> regulated by DNA methylation at cg21568453 may promote the occurrence of bronchiectasis.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2521622"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12184172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decitabine-induced DNA methylation remodeling reveals targetable biological processes in gilthead seabream pituitary and liver explants.","authors":"E Perera, C Navarro-Guillén, J Román-Padilla, R Huesa-Cerdán, J A Hidalgo-Perez, J A Martos-Sitcha, G Martínez-Rodríguez, Daniel Alpízar-Pedraza, Jorge M O Fernandes, Javier A Rodriguez-Casariego","doi":"10.1080/15592294.2025.2566515","DOIUrl":"10.1080/15592294.2025.2566515","url":null,"abstract":"<p><p>Epigenetic manipulations have the potential to improve traits in farmed fish. To explore this opportunity in the gilthead seabream (<i>Sparus aurata</i>), the catalytic domains of five DNA methyltransferases (DNMTs) were predicted by homology modeling, and their interaction with the inhibitor 5-aza-2'-deoxycytidine (DAC) was assessed by docking, revealing that the inhibitor can bind all DNMTs with similar energy. Then, pituitary and liver explants from gilthead seabream were exposed to DAC for 24 h, and changes in genome-wide DNA methylation (RRBS) and gene expression (RNA-seq) were assessed. In the liver, functional enrichment revealed upregulation of ribosome biogenesis and protein synthesis, while mitochondrial functioning, genome stability, and DNA and amino acid metabolism were downregulated. Exposed pituitaries displayed upregulation of ribosomal biogenesis and protein synthesis, alongside mitochondrial functioning and genome stability. Nucleotide-level methylomes were obtained for the first time in this species, with hypomethylated sites observed in 3'UTRs, promoter regions, and introns of highly expressed genes across both tissues. A higher level of DNA methylation at exons was found in highly expressed genes in the liver. The seabream pituitary was more permissive to DNA methylation remodeling than the liver. Functional Epigenetic Module analysis revealed seven interactome hotspots in liver and four in pituitary, mostly related to protein trafficking and signal transduction in the liver, and mitochondrial functioning in the pituitary, indicating that these functions can potentially be targeted by epigenetic interventions in seabream. The data resources generated in our study may be used to explore novel avenues to boost seabream performance and welfare.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2566515"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12505512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145243914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insight into the mechanisms and dysregulation of KMT5C-H4K20me3 in cancer.","authors":"Jihye Son, Andrea L Kasinski","doi":"10.1080/15592294.2025.2574007","DOIUrl":"https://doi.org/10.1080/15592294.2025.2574007","url":null,"abstract":"<p><p>KMT5C-mediated histone H4 lysine 20 trimethylation (H4K20me3) has traditionally been linked to heterochromatin formation and maintenance, playing a crucial role in maintaining genome integrity. Emerging evidence, however, indicates that perturbations of KMT5C-H4K20me3 are also implicated in various cancers, positioning KMT5C-H4K20me3 as a promising target for anti-cancer therapies. Despite this, the precise mechanisms underlying KMT5C recruitment to its genomic targets and the specific genes it regulates remain poorly understood. In this review, we explore the dysregulation of KMT5C-mediated H4K20me3 in cancer, providing a comprehensive overview of its known functions. We also highlight recent findings that suggest a novel, non-canonical pathway for H4K20me3 deposition by KMT5C, and, while early on, insight into future opportunities for therapeutic intervention.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2574007"},"PeriodicalIF":3.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145312630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive analysis of eccDNA characteristics and associated genes expression in peripheral blood of ASLE and ISLE patients.","authors":"Yali Peng, Huihui Tao, Dongzhou Liu, Donger Tang, Chunmei Wen, Mengyao Wu, Tiantian Xu, Guoying Wang, Xuejia Zheng, Yong Dai","doi":"10.1080/15592294.2025.2477903","DOIUrl":"10.1080/15592294.2025.2477903","url":null,"abstract":"<p><p>To explore SLE staging markers, we analyzed eccDNA in plasma using circular sequencing, comparing healthy controls (HC), active SLE (ASLE), and inactive SLE (ISLE) patients. We found higher eccDNA levels and lower GC content in ASLE and ISLE compared to healthy controls, with a negative correlation between GC content and anti-daDNA, C3, and C4 levels in SLE and HC samples. Differential expression of exon-derived eccGenes in ASLE and ISLE suggests their role in SLE development, with KEGG analysis showing enrichment in SLE-related pathways for these differentially expressed genes. By protein-protein interactions network analysis we found 9 exon-derived eccGenes that were significantly differentially expressed and scored high in both ISLE-HC and ASLE-ISLE as diagnostic criteria for differentiating different disease stages of SLE. In conclusion, the present study reveals that eccDNA length GC content as well as chromosomal distribution in ASLE, ISLE and HC suggests that with eccDNA is associated with the creation of SLE, suggesting GC count of eccDNA as a diagnostic marker for systemic lupus erythematosus. Significant changes in the abundance of eccDNA-related genes from exons such as SOS1, GAD2, BCL11B, PPT1, and GCNT3 were observed in ISLE as compared to ASLE and HC groups and were significantly correlated with SLEDAI-2K. This suggests that these exon-derived eccGenes may play a role in the development and progression of the disease. Consequently, the abundance levels of these exon-derived eccGenes could potentially assist in distinguishing different stages of SLE, beyond a confirmed diagnosis, thus serving as possible biomarkers for the condition.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2477903"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11926905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143662872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA methylation heterogeneity attributable to a complex tumor immune microenvironment prompts prognostic risk in glioma.","authors":"Shuangyue Ma, Xu Pan, Jing Gan, Xiaxin Guo, Jiaheng He, Haoyu Hu, Yuncong Wang, Shangwei Ning, Hui Zhi","doi":"10.1080/15592294.2024.2318506","DOIUrl":"10.1080/15592294.2024.2318506","url":null,"abstract":"<p><p>Gliomas are malignant tumours of the human nervous system with different World Health Organization (WHO) classifications, glioblastoma (GBM) with higher grade and are more malignant than lower-grade glioma (LGG). To dissect how the DNA methylation heterogeneity in gliomas is influenced by the complex cellular composition of the tumour immune microenvironment, we first compared the DNA methylation profiles of purified human immune cells and bulk glioma tissue, stratifying three tumour immune microenvironmental subtypes for GBM and LGG samples from The Cancer Genome Atlas (TCGA). We found that more intermediate methylation sites were enriched in glioma tumour tissues, and used the Proportion of sites with Intermediate Methylation (PIM) to compare intertumoral DNA methylation heterogeneity. A larger PIM score reflected stronger DNA methylation heterogeneity. Enhanced DNA methylation heterogeneity was associated with stronger immune cell infiltration, better survival rates, and slower tumour progression in glioma patients. We then created a Cell-type-associated DNA Methylation Heterogeneity Contribution (CMHC) score to explore the impact of different immune cell types on heterogeneous CpG site (<i>CpG</i>^<i>ct</i>) in glioma tissues. We identified eight prognosis-related <i>CpG</i>^<i>ct</i> to construct a risk score: the Cell-type-associated DNA Methylation Heterogeneity Risk (CMHR) score. CMHR was positively correlated with cytotoxic T-lymphocyte infiltration (CTL), and showed better predictive performance for IDH status (AUC = 0.96) and glioma histological phenotype (AUC = 0.81). Furthermore, DNA methylation alterations of eight <i>CpG</i>^<i>ct</i> might be related to drug treatments of gliomas. In conclusion, we indicated that DNA methylation heterogeneity is associated with a complex tumour immune microenvironment, glioma phenotype, and patient's prognosis.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"19 1","pages":"2318506"},"PeriodicalIF":3.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10936651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140027750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Calling the question: what is mammalian transgenerational epigenetic inheritance?","authors":"Hasan Khatib, Jessica Townsend, Melissa A Konkel, Gabi Conidi, Julia A Hasselkus","doi":"10.1080/15592294.2024.2333586","DOIUrl":"10.1080/15592294.2024.2333586","url":null,"abstract":"<p><p>While transgenerational epigenetic inheritance has been extensively documented in plants, nematodes, and fruit flies, its existence in mammals remains controversial. Several factors have contributed to this debate, including the lack of a clear distinction between intergenerational and transgenerational epigenetic inheritance (TEI), the inconsistency of some studies, the potential confounding effects of in-utero vs. epigenetic factors, and, most importantly, the biological challenge of epigenetic reprogramming. Two waves of epigenetic reprogramming occur: in the primordial germ cells and the developing embryo after fertilization, characterized by global erasure of DNA methylation and remodelling of histone modifications. Consequently, TEI can only occur if specific genetic regions evade this reprogramming and persist through embryonic development. These challenges have revived the long-standing debate about the possibility of inheriting acquired traits, which has been strongly contested since the Lamarckian and Darwinian eras. As a result, coupled with the absence of universally accepted criteria for transgenerational epigenetic studies, a vast body of literature has emerged claiming evidence of TEI. Therefore, the goal of this study is to advocate for establishing fundamental criteria that must be met for a study to qualify as evidence of TEI. We identified five criteria based on the consensus of studies that critically evaluated TEI. To assess whether published original research papers adhere to these criteria, we examined 80 studies that either claimed or were cited as supporting TEI. The findings of this analysis underscore the widespread confusion in this field and highlight the urgent need for a unified scientific consensus on TEI requirements.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"19 1","pages":"2333586"},"PeriodicalIF":3.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10965103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140206498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-coding 886 (<i>nc886</i>/<i>vtRNA2-1</i>), the epigenetic odd duck - implications for future studies.","authors":"Emma Raitoharju, Sonja Rajić, Saara Marttila","doi":"10.1080/15592294.2024.2332819","DOIUrl":"10.1080/15592294.2024.2332819","url":null,"abstract":"<p><p>Non-coding 886 (<i>nc886</i>, <i>vtRNA2-1</i>) is the only human polymorphically imprinted gene, in which the methylation status is not determined by genetics. Existing literature regarding the establishment, stability and consequences of the methylation pattern, as well as the nature and function of the <i>nc886</i> RNAs transcribed from the locus, are contradictory. For example, the methylation status of the locus has been reported to be stable through life and across somatic tissues, but also susceptible to environmental effects. The nature of the produced <i>nc886</i> RNA(s) has been redefined multiple times, and in carcinogenesis, these RNAs have been reported to have conflicting roles. In addition, due to the bimodal methylation pattern of the <i>nc886</i> locus, traditional genome-wide methylation analyses can lead to false-positive results, especially in smaller datasets. Herein, we aim to summarize the existing literature regarding <i>nc886</i>, discuss how the characteristics of <i>nc886</i> give rise to contradictory results, as well as to reinterpret, reanalyse and, where possible, replicate the results presented in the current literature. We also introduce novel findings on how the distribution of the <i>nc886</i> methylation pattern is associated with the geographical origins of the population and describe the methylation changes in a large variety of human tumours. Through the example of this one peculiar genetic locus and RNA, we aim to highlight issues in the analysis of DNA methylation and non-coding RNAs in general and offer our suggestions for what should be taken into consideration in future analyses.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"19 1","pages":"2332819"},"PeriodicalIF":3.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10965113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140206526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}