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Study on the molecular mechanism of dietary FCE supplementation in regulating chicken meat quality 饲粮中添加FCE调节鸡肉品质的分子机制研究。
IF 2.4 3区 生物学 Q2 GENETICS & HEREDITY Pub Date : 2026-01-20 Epub Date: 2025-10-30 DOI: 10.1016/j.gene.2025.149865
Wei Zhao, Jinli Tian, Lijuan Yang, Lin Xue, Siyu Chen, Rinmin Ma, Yaling Gu, Dawei Wei, Juan Zhang
Meat quality is a critical factor influencing the sales of chicken. Most plant extracts have been shown to improve meat quality in poultry. This study selected 120 similar-weight (1.5 ± 0.2 kg) 135-day-old Jingyuan chickens, divided them into four groups, and fed them different doses (CON, 0.3 % FCE, 0.6 % FCE, and 0.9 % FCE) of fresh corn extract (FCE) until they were 180-day-old chickens. Fifteen chickens were randomly selected from each group for slaughter performance and meat quality assessment. Combining the transcriptome and metabolome sequencing data of the breast (CON and 0.6 % FCE), the weighted co-expression network analysis (WGCNA) method was used to identify hub genes and key metabolites significantly related to meat quality. The results showed that the 0.6 % FCE group was significantly better than the other groups in terms of slaughter performance and meat quality. Transcriptomic analysis identified differentially expressed genes (DEGs) significantly enriched in mineral absorption, amino sugar and nucleotide sugar metabolism, and phosphonate and phosphinate metabolism. Based on WGCNA, six key DEGs significantly associated with meat quality were selected. Metabolomics analysis identified differentially expressed metabolites (DEMs) significantly enriched in the pathways of secondary bile acid biosynthesis, autophagy, pantothenate and CoA biosynthesis, and beta-alanine metabolism Pearson correlation analysis further revealed correlations between the six key DEGs (YKT6, ENSGALG00010016848, GALK2, COMMD9, EIF2D, and GABPB2) and five key DEMs (1H-Indole-4-carboxaldehyde, Leucylproline, Trimethoprim, Ursodeoxycholic acid, and N.epsilon.-Acetyl-L-lysine). Furthermore, the expression levels and content of these genes and metabolites in the breast muscle of Jingyuan chickens were also assessed.
肉质是影响鸡肉销售的关键因素。大多数植物提取物已被证明能改善家禽的肉质。本试验选取体重相近(1.5 ± 0.2 kg)的135日龄靖远鸡120只,分为4组,分别饲喂不同剂量(CON、0.3 % FCE、0.6 % FCE和0.9 % FCE)的新鲜玉米提取物(FCE)至180日龄。每组随机选取15只鸡进行屠宰性能和肉质评价。结合乳腺转录组和代谢组测序数据(CON和0.6 % FCE),采用加权共表达网络分析(WGCNA)方法,鉴定与肉品质显著相关的枢纽基因和关键代谢物。结果表明,0.6 % FCE组屠宰性能和肉质均显著优于其他各组。转录组学分析发现,差异表达基因(DEGs)在矿物质吸收、氨基糖和核苷酸糖代谢、磷酸盐和膦酸盐代谢中显著富集。基于WGCNA,选择了6个与肉质性状显著相关的关键deg。代谢组学分析发现,在次生胆囊酸生物合成、自噬、泛酸和辅酶a生物合成途径中显著富集的差异表达代谢物(DEMs), β -丙氨酸代谢Pearson相关分析进一步揭示了6个关键DEGs (YKT6、ENSGALG00010016848、GALK2、COMMD9、EIF2D和GABPB2)与5个关键DEMs (1h -吲哚-4-甲醛、Leucylproline、Trimethoprim、Ursodeoxycholic acid、和N.epsilon.-Acetyl-L-lysine)。此外,还对这些基因和代谢物在靖远鸡胸肌中的表达水平和含量进行了评价。
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引用次数: 0
Expression analysis of androglobin and its influence on the transcriptome in cancer 雄性红蛋白在肿瘤组织中的表达分析及其对转录组的影响。
IF 2.4 3区 生物学 Q2 GENETICS & HEREDITY Pub Date : 2026-01-20 Epub Date: 2025-10-24 DOI: 10.1016/j.gene.2025.149840
Carina Osterhof , Michel Seiwert , Stefan Mündnich , Teng Wei Koay , Elena Porto , Glen Kristiansen , David Hoogewijs , Thomas Hankeln
Androglobin (ADGB) is a phylogenetically ancient multi-domain protein with an embedded globin domain, which binds heme and may therefore interact with gaseous molecules. Other globins like neuroglobin, cytoglobin and myoglobin have shown tumor-suppressor or oncogenic roles in a tissue-dependent way, and also ADGB has been suggested as being oncogenic in prostate and brain cancer models. However, ADGB expression in human tumor entities in vivo has not been investigated systematically so far. Here we mined transcriptome data from various cancer types and reveal that ADGB is typically downregulated in cancer cell lines, as well as in tumors from lung and testis, which express ADGB endogenously in healthy states. We show via bioinformatics analyses that in cell lines only a few ADGB exons are transcribed, or the gene locus was amplified, which greatly limits suitability of such cell lines as model systems for research into ADGB. Consistent with correlation analysis, we further demonstrate that RFX3 regulates ADGB promoter-driven luciferase activity as well as endogenous ADGB expression levels. Since recent literature postulated oncogenic effects of ADGB, we established stable ADGB overexpression (ADGB+) in A549 lung cancer cells. Our transcriptomic analysis of ADGB + cells indicate increased cell motility and restructuring of the extracellular matrix – both hallmarks of elevated malignancy. ADGB thus may display oncogenic potential in vitro. However, since human cancer entities show little to no ADGB transcription, a role for ADGB in tumorigenesis in vivo appears rather limited.
Androglobin (ADGB)是一种具有嵌入式珠蛋白结构域的古老多结构域蛋白,与血红素结合,因此可能与气体分子相互作用。其他珠蛋白如神经珠蛋白、细胞珠蛋白和肌红蛋白以组织依赖的方式显示出肿瘤抑制或致癌作用,ADGB也被认为在前列腺癌和脑癌模型中具有致癌作用。然而,到目前为止,ADGB在人体肿瘤实体中的表达还没有系统的研究。在这里,我们挖掘了来自各种癌症类型的转录组数据,发现ADGB在癌细胞系以及肺和睾丸肿瘤中通常是下调的,这些肿瘤在健康状态下内源性表达ADGB。我们通过生物信息学分析表明,在细胞系中,只有少数ADGB外显子被转录,或者基因位点被扩增,这极大地限制了这些细胞系作为ADGB研究模型系统的适用性。与相关分析一致,我们进一步证明RFX3调节ADGB启动子驱动的荧光素酶活性以及内源性ADGB表达水平。由于最近的文献假设了ADGB的致癌作用,我们在A549肺癌细胞中建立了稳定的ADGB过表达(ADGB + )。我们对ADGB + 细胞的转录组学分析表明,细胞运动性和细胞外基质的重组增加,这两者都是恶性肿瘤升高的标志。因此,ADGB在体外可能显示出致癌潜力。然而,由于人类癌症实体很少或没有ADGB转录,ADGB在体内肿瘤发生中的作用似乎相当有限。
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引用次数: 0
β-catenin/TCF4/NANOG axis controls miR-302 transcription in colorectal cancer cells β-catenin/TCF4/NANOG轴控制结直肠癌细胞中miR-302的转录。
IF 2.4 3区 生物学 Q2 GENETICS & HEREDITY Pub Date : 2026-01-20 Epub Date: 2025-11-10 DOI: 10.1016/j.gene.2025.149890
Kiarash Saleki , Miao Xue , Amirreza Mazloomi , Bradley Spencer-Dene , Abdolrahman S. Nateri
The miR-302 cluster, a key pluripotency-associated non-coding RNA, has been implicated in stem cell homeostasis and tumourigenesis. However, its regulatory mechanisms in cancers, including colorectal cancer (CRC) remain poorly understood. Here, we demonstrate that the β-catenin/TCF4 complex significantly enhances miR-302 expression through direct promoter activation in CRC cells. We hypothesized that the β-catenin/TCF4 complex directly activates the miR-302 promoter and cooperates with NANOG in a transcriptional feedback loop sustaining stem-like traits in CRC cells. Using a combination of promoter-driven luciferase reporter assays, chromatin immunoprecipitation (ChIP), and molecular dynamics simulations, we identify a regulatory axis involving Wnt signalling and the transcription factor NANOG. Our data show that individual members of the miR-302 cluster activate the NANOG promoter, while both NANOG and β-catenin/TCF4 synergistically enhance miR-302 promoter activity, suggesting the presence of a positive feedback loop. Structural simulations further elucidate the binding interactions between TCF4, NANOG, and the miR-302 promoter, corroborating our experimental observations. Together, these findings position miR-302 as a downstream effector of Wnt/β-catenin signalling and an integral component of NANOG-mediated transcriptional networks in CRC stem-like cells. This work advances our understanding of non-coding RNA regulation in cancer and highlights potential therapeutic opportunities for targeting stemness-associated pathways.
miR-302簇是一种关键的多能性相关非编码RNA,与干细胞稳态和肿瘤发生有关。然而,其在包括结直肠癌(CRC)在内的癌症中的调节机制仍然知之甚少。在这里,我们证明β-catenin/TCF4复合物通过直接启动子激活在CRC细胞中显著增强miR-302的表达。我们假设β-catenin/TCF4复合物直接激活miR-302启动子,并在维持CRC细胞干样性状的转录反馈回路中与NANOG合作。通过结合启动子驱动的荧光素酶报告子测定、染色质免疫沉淀(ChIP)和分子动力学模拟,我们确定了一个涉及Wnt信号和转录因子NANOG的调控轴。我们的数据显示,miR-302集群的单个成员激活NANOG启动子,而NANOG和β-catenin/TCF4协同增强miR-302启动子活性,表明存在正反馈回路。结构模拟进一步阐明了TCF4、NANOG和miR-302启动子之间的结合相互作用,证实了我们的实验观察。总之,这些发现表明miR-302是Wnt/β-catenin信号传导的下游效应因子,也是CRC干细胞样细胞中nanog介导的转录网络的一个组成部分。这项工作促进了我们对癌症中非编码RNA调控的理解,并强调了针对干细胞相关途径的潜在治疗机会。
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引用次数: 0
Functional analysis of two component signaling system in Mycobacterium tuberculosis 结核分枝杆菌双组分信号系统的功能分析。
IF 2.4 3区 生物学 Q2 GENETICS & HEREDITY Pub Date : 2026-01-20 Epub Date: 2025-11-07 DOI: 10.1016/j.gene.2025.149868
Karthikeyan Sundaram , Sridhar Rathinam
Tuberculosis is a fatal infection transmitted through airborne droplet nuclei. The etiological agent is Mycobacterium tuberculosis, an acid-fast bacillus. Drug-resistant tuberculosis poses a global challenge, with specific mycobacterial genes intricately associated with drug resistance. Numerous factors are implicated in the etiology of the condition. This review specifically aims to examine ClpCP, an ATPase belonging to the AAA + protease family, and the genes of the two-component sensor system related with disease etiology. Mycobacterium TB depends significantly on protein degradation to regulate their quantity and quality, which is crucial for its proliferation and pathogenicity involving Clp. The two-component sensor system comprises histidine kinase (HK) and response regulator (RR), which governs responses to stress situations, starvation, nutritional abundance, persistence, hypoxia, dormancy, and primarily disease pathogenesis. Within the two-component system, there exist 12 pairs, including SenX3/RegX3, PhoP/PhoR, DosR/DosS, MtrA/MtrB, and PdtaS/PdtaR, alongside 6 response regulators Rv0195, Rv0260c, Rv0818, PdtaR, Rv2884, and Rv3143 encoded in the Mycobacterium tuberculosis genome. The PhoPR genes have been extensively researched, and the pathogenicity of Mycobacterium tuberculosis (MTB) is contingent upon the sensor kinase of the PhoPR two-component regulatory system, known as PhoR. This review will examine the roles of genes related to the factors associated with mycobacterial growth and pathogenesis.
结核病是一种通过空气传播的飞沫核传播的致命传染病。病原是结核分枝杆菌,一种抗酸杆菌。耐药结核病是一项全球性挑战,特定的分枝杆菌基因与耐药有着错综复杂的关系。许多因素涉及到该病的病因学。这篇综述特别旨在研究ClpCP,一种属于AAA + 蛋白酶家族的atp酶,以及与疾病病因相关的双组分传感器系统基因。结核分枝杆菌主要依靠蛋白质降解来调节其数量和质量,这对其涉及Clp的增殖和致病性至关重要。这种双组分传感器系统包括组氨酸激酶(HK)和反应调节因子(RR),它们控制对应激情况、饥饿、营养丰富、持久性、缺氧、休眠和主要疾病发病机制的反应。在双组分体系中,共编码SenX3/RegX3、PhoP/PhoR、DosR/DosS、MtrA/MtrB、PdtaS/PdtaR等12对,以及Rv0195、Rv0260c、Rv0818、PdtaR、Rv2884、Rv3143 6个应答调控因子。PhoPR基因已被广泛研究,结核分枝杆菌(MTB)的致病性取决于PhoPR双组分调控系统(PhoR)的传感器激酶。本文将探讨与分枝杆菌生长和发病相关的基因的作用。
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引用次数: 0
Role of myocardium-derived exosomal miRNAs in doxorubicin-induced cardiomyopathy 心肌源性外泌体mirna在阿霉素诱导的心肌病中的作用。
IF 2.4 3区 生物学 Q2 GENETICS & HEREDITY Pub Date : 2026-01-20 Epub Date: 2025-10-20 DOI: 10.1016/j.gene.2025.149842
Cui Li , Yudie Song , Binbin Cao , Jiahui Li , Fan Xu , Weiping Du , Zhaoxia Zhang , Binjie Su , Xiaomin Chen , Qinglin Yu , Jia Su

Background

Doxorubicin-induced cardiomyopathy (DCM) remains a major clinical challenge, highlighting the need for early diagnostic biomarkers. Exosomal miRNAs are promising candidates due to their stability and regulatory functions in cardiovascular diseases.

Methods

Exosomes were isolated from myocardial tissue samples of DOX-treated and control rats using differential ultracentrifugation and were subsequently characterized by transmission electron microscopy, Western blotting, and nanoparticle tracking analysis. Differentially expressed miRNAs were screened by microarray analysis. The miRanda algorithm was used to predict target genes, followed by functional enrichment analysis. qRT‒PCR validated selected miRNAs and their target genes.

Results

Doxorubicin administration induced significant cardiac dysfunction, characterized by decreased left ventricular ejection fraction (LVEF) and increased serum levels of cardiac biomarkers (cTnI, BNP, and CK-MB). Microarray profiling revealed 26 differentially expressed miRNAs, and KEGG enrichment analysis indicated enrichment in the MAPK signaling pathway. qRT‒PCR demonstrated upregulation of exosomal miR-182 and downregulation of Taok2 mRNA, a key MAPK gene. ROC analysis indicated the potential of exosomal miR-182 for DCM diagnosis.

Conclusion

Exosomal miR-182 may serve as a diagnostic marker for DCM. Bioinformatic analyses predict its potential regulation of the MAPK pathway through Taok2 targeting, although this mechanistic relationship requires experimental validation. These findings provide new perspectives for the early monitoring of DCM.
背景:阿霉素诱导的心肌病(DCM)仍然是一个主要的临床挑战,突出了对早期诊断生物标志物的需求。外泌体mirna因其在心血管疾病中的稳定性和调节作用而成为有希望的候选者。方法:采用差示超离心方法从dox处理和对照大鼠心肌组织样本中分离外泌体,随后采用透射电镜(TEM)、免疫印迹(Western blotting)和纳米颗粒跟踪分析(NTA)对其进行表征。通过微阵列分析筛选差异表达的mirna。使用miRanda算法预测目标基因,然后进行功能富集分析。qRT-PCR验证了所选的mirna及其靶基因。结果:阿霉素引起了明显的心功能障碍,其特征是左心室射血分数(LVEF)降低,血清心脏生物标志物(cTnI、BNP和CK-MB)水平升高。微阵列分析显示了26个差异表达的mirna, KEGG富集分析表明在MAPK信号通路中富集。qRT-PCR显示外泌体miR-182上调,MAPK关键基因Taok2 mRNA下调。ROC分析显示外泌体miR-182诊断DCM的潜力。结论:外泌体miR-182可作为DCM的诊断标志物。生物信息学分析预测其可能通过Taok2靶向调控MAPK通路,尽管这种机制关系需要实验验证。这些发现为DCM的早期监测提供了新的视角。
{"title":"Role of myocardium-derived exosomal miRNAs in doxorubicin-induced cardiomyopathy","authors":"Cui Li ,&nbsp;Yudie Song ,&nbsp;Binbin Cao ,&nbsp;Jiahui Li ,&nbsp;Fan Xu ,&nbsp;Weiping Du ,&nbsp;Zhaoxia Zhang ,&nbsp;Binjie Su ,&nbsp;Xiaomin Chen ,&nbsp;Qinglin Yu ,&nbsp;Jia Su","doi":"10.1016/j.gene.2025.149842","DOIUrl":"10.1016/j.gene.2025.149842","url":null,"abstract":"<div><h3>Background</h3><div>Doxorubicin-induced cardiomyopathy (DCM) remains a major clinical challenge, highlighting the need for early diagnostic biomarkers. Exosomal miRNAs are promising candidates due to their stability and regulatory functions in cardiovascular diseases.</div></div><div><h3>Methods</h3><div>Exosomes were isolated from myocardial tissue samples of DOX-treated and control rats using differential ultracentrifugation and were subsequently characterized by transmission electron microscopy, Western blotting, and nanoparticle tracking analysis. Differentially expressed miRNAs were screened by microarray analysis. The miRanda algorithm was used to predict target genes, followed by functional enrichment analysis. qRT‒PCR validated selected miRNAs and their target genes.</div></div><div><h3>Results</h3><div>Doxorubicin administration induced significant cardiac dysfunction, characterized by decreased left ventricular ejection fraction (LVEF) and increased serum levels of cardiac biomarkers (cTnI, BNP, and CK-MB). Microarray profiling revealed 26 differentially expressed miRNAs, and KEGG enrichment analysis indicated enrichment in the MAPK signaling pathway. qRT‒PCR demonstrated upregulation of exosomal miR-182 and downregulation of Taok2 mRNA, a key MAPK gene. ROC analysis indicated the potential of exosomal miR-182 for DCM diagnosis.</div></div><div><h3>Conclusion</h3><div>Exosomal miR-182 may serve as a diagnostic marker for DCM. Bioinformatic analyses predict its potential regulation of the MAPK pathway through Taok2 targeting, although this mechanistic relationship requires experimental validation. These findings provide new perspectives for the early monitoring of DCM.</div></div>","PeriodicalId":12499,"journal":{"name":"Gene","volume":"977 ","pages":"Article 149842"},"PeriodicalIF":2.4,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145336825","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}
引用次数: 0
NR1D1 in tumorigenesis: dual roles, mechanisms, and therapeutic targeting NR1D1在肿瘤发生中的双重作用、机制和治疗靶向。
IF 2.4 3区 生物学 Q2 GENETICS & HEREDITY Pub Date : 2026-01-20 Epub Date: 2025-11-09 DOI: 10.1016/j.gene.2025.149889
Zhuangwei Lv , Ruohao Yang , Jinhua Wu , Xiaoyu Shi , Ruihan Wang , Yi’ang Niu , Zhuang Qian , Junna Jiao , Yunfeng Ma
Nuclear receptor subfamily 1, group D, member 1 (NR1D1, also known as REV-ERBα), a core circadian regulator, plays context-dependent dual roles in cancer, acting as either a tumor suppressor or oncogene. This review synthesizes current evidence on NR1D1’s regulation of key oncogenic pathways: DNA repair, immunomodulation (e.g., the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway, NOD-like receptor family pyrin domain containing 3(NLRP3)), metabolism, and signaling cascades such as PI3K/AKT, JAK/STAT. We highlight its clinical utility as a prognostic biomarker and therapeutic target, focusing on pharmacological modulators with demonstrated preclinical efficacy. We also critically discuss challenges in targeting NR1D1 and its potential in combination therapies, offering new insights for cancer treatment.
核受体亚家族1,D组,成员1 (NR1D1,也称为rev - erba),是一个核心的昼夜节律调节因子,在癌症中起着环境依赖的双重作用,既可以作为肿瘤抑制因子,也可以作为致癌基因。本文综述了NR1D1调控主要致癌通路的现有证据:DNA修复、免疫调节(如环GMP-AMP合成酶(cGAS)-干扰素基因刺激因子(STING)通路、nod样受体家族pyrin结构域3(NLRP3))、代谢和信号级联如PI3K/AKT、JAK/STAT。我们强调其作为预后生物标志物和治疗靶点的临床应用,重点关注具有临床前疗效的药理学调节剂。我们还批判性地讨论了靶向NR1D1的挑战及其在联合治疗中的潜力,为癌症治疗提供了新的见解。
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引用次数: 0
Genomic plasticity and phylogeny of sheeppox and goatpox viruses reveal progressive host and terrestrial adaptation 绵羊痘和山羊痘病毒的基因组可塑性和系统发育揭示了逐步的宿主和陆地适应。
IF 2.4 3区 生物学 Q2 GENETICS & HEREDITY Pub Date : 2026-01-20 Epub Date: 2025-11-03 DOI: 10.1016/j.gene.2025.149869
Rajesh Chahota, Tania Gupta, Mandeep Sharma, Subhash Verma, Prasenjit Dhar, Monika Bhardwaj, Vanita Patial
Sheeppox virus (SPPV) and Goatpox virus (GTPV), members of the genus Capripoxvirus, cause transboundary pox diseases in sheep and goats. Although disease is mostly host-specific, uncertainty of cross-infection always exists under mixed farming practices. A comprehensive genome-wide plasticity and phylogenetic analysis was performed by comparing 17 SPPV and 11 GTPV field strains with host-specific native SPPV-SP3-Nur and GTPV-GP5-Indora strains. Compared to the reference strains, SPPV TU-V02127 (NC_004002.1) and GTPV Pellor (NC_004003.1), both native strains showed genetically conserved core genes with variations concentrated in terminal regions genes linked to virulence and host interaction (B22R-like protein, kelch- like protein, serpins, ankyrin repeat proteins). The majority of studied SPPV and GTPV strains maintained strong genomic stability, except for a GTPV Yemen strain, for which cross-species (host) infection was reported, and a few strains showed evidence of frequent involvement as minor parents in interspecies recombination within highly plastic regions containing genes for immune evasion and host determinants. Phylogenetic analysis of 28 complete genomes showed host-specific, territory-definite clades and subclades with SP3-Nur and GP5-Indora clustering within the Asian subclade S2.3 and G1.1, respectively, representing Indian regional subclades. This study highlights the progressive host as well as terrestrial adaptation of SPPV and GTPV in general. Though the existence of strains with high genomic plasticity may be a localised and evolving high-risk phenomenon at present, it poses a larger threat of transboundary and cross-species spread. These findings underscore the need for wider genomic surveillance to monitor viral transmission and tracking transboundary spread for effective disease management.
羊痘病毒(SPPV)和山羊痘病毒(GTPV)是山羊痘病毒属的成员,可在绵羊和山羊中引起跨界痘病。虽然疾病主要是宿主特异性的,但在混合耕作方式下,交叉感染的不确定性始终存在。将17株SPPV和11株GTPV田间菌株与宿主特异性本地菌株SPPV- sp3 - nur和GTPV- gp5 - indora进行了全面的全基因组可塑性和系统发育分析。与参考菌株SPPV TU-V02127 (NC_004002.1)和GTPV Pellor (NC_004003.1)相比,两种本地菌株均显示遗传保守的核心基因,变异集中在与毒力和宿主相互作用相关的末端区域基因(B22R-like蛋白、kelch- like蛋白、serpins、锚蛋白重复蛋白)。大多数研究的SPPV和GTPV菌株保持了很强的基因组稳定性,除了也门的GTPV菌株报道了跨物种(宿主)感染,少数菌株在含有免疫逃避基因和宿主决定因素的高度可塑性区域内经常作为次要亲本参与种间重组。28个全基因组的系统发育分析显示,在亚洲亚支系S2.3和G1.1中,SP3-Nur和GP5-Indora聚类分别代表了印度区域亚支系。本研究强调了SPPV和GTPV的宿主进行性和陆地适应性。虽然目前具有高基因组可塑性的菌株的存在可能是一种局部的、不断进化的高风险现象,但它对跨界和跨种传播构成了更大的威胁。这些发现强调需要进行更广泛的基因组监测,以监测病毒传播和追踪跨界传播,从而实现有效的疾病管理。
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引用次数: 0
Retraction notice to “Genetic variations of prostate stem cell antigen (PSCA) contribute to the risk of gastric cancer for Eastern Asians: a Meta-analysis based on 16792 individuals”. [Gene 493 (2012) 83–91] “前列腺干细胞抗原(PSCA)的遗传变异与东亚人患胃癌的风险有关:一项基于16792人的荟萃分析”的撤回通知。[基因493(2012)83-91]。
IF 2.4 3区 生物学 Q2 GENETICS & HEREDITY Pub Date : 2026-01-15 Epub Date: 2025-11-17 DOI: 10.1016/j.gene.2025.149823
Lei Qiao, Yong Feng
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引用次数: 0
Intramyocardial baculovirus-Meis1 gene therapy induces angio-arteriogenesis in sheep with myocardial infarction 心内杆状病毒- meis1基因治疗诱导心肌梗死绵羊血管动脉生成。
IF 2.4 3区 生物学 Q2 GENETICS & HEREDITY Pub Date : 2026-01-15 Epub Date: 2025-11-01 DOI: 10.1016/j.gene.2025.149867
Ayelén Emilce López , Paola Locatelli , Jorge Alejandro Simonin , Mariano Nicolás Belaich , Agustina Scharn , Alberto José Crottogini , Fernanda Daniela Olea , María del Rosario Bauzá

Background

Ischemic heart disease is the cardiovascular condition with the highest morbidity and mortality worldwide, highlighting the need for therapies aimed at promoting neovascularization of the ischemic myocardium. Given the involvement of the transcription factor Myeloid ecotropic viral integration site 1 (MEIS1) in the development of the vascular network in vertebrates, we hypothesized that MEIS1 overexpression would induce microvascular proliferation in an ovine model of acute myocardial infarction.

Methods

A baculoviral vector encoding MEIS1 (Bv.Meis1) was designed and injected into the peri-infarct zone of adult sheep with permanent coronary ligation. Control sheep were injected with an empty baculovirus (Bv.Null). One week later, microvascular densities and expression of angiogenic genes were assessed in myocardial tissue samples.

Results

Animals treated with Bv.Meis1 exhibited significantly greater capillary and arteriolar densities as well as a significant increase in the expression of Vegf, Angiogenin, Hif1α, Igf, Fgf2 and Prok2, compared to Bv.Null group. Additionally, overexpression of most of these genes was also found in cultures of neonatal rat cardiomyocytes transduced with Bv.Meis1, and increased tubulogenesis was observed in HMEC-1 cells incubated with supernatants of these cultures. Finally, the vector’s biosafety was demonstrated by the absence of viral DNA expression in tissues remote to the heart.

Conclusions

Intramyocardial injection of a baculovirus encoding MEIS1 promotes overexpression of angiogenic genes which, in turn, induce angio-arteriogenesis in ovine myocardial infarction. Given the highly translational nature of the animal model and the good biosafety profile of the baculoviral vector, this strategy could potentially be useful for patients with ischemic heart disease.
背景:缺血性心脏病是世界范围内发病率和死亡率最高的心血管疾病,强调了促进缺血性心肌新生血管的治疗需求。鉴于转录因子髓系嗜生态病毒整合位点1 (MEIS1)参与脊椎动物血管网络的发育,我们假设MEIS1过表达会诱导绵羊急性心肌梗死模型的微血管增殖。方法:设计一种编码MEIS1的杆状病毒载体(Bv.Meis1),并将其注射到永久性冠脉结扎的成年绵羊梗死周围区。对照羊注射空杆状病毒(Bv.Null)。一周后,检测心肌组织样本微血管密度和血管生成基因的表达。结果:Bv治疗动物。与Bv相比,Meis1的毛细血管和小动脉密度显著增加,Vegf、Angiogenin、Hif1α、Igf、Fgf2和Prok2的表达显著增加。零组。此外,在Bv转导的新生大鼠心肌细胞培养中也发现了大多数这些基因的过表达。HMEC-1细胞与这些培养物的上清液孵育后,观察到微管形成增加。最后,通过在远离心脏的组织中不表达病毒DNA,证明了载体的生物安全性。结论:心内注射编码MEIS1的杆状病毒可促进血管生成基因的过度表达,从而诱导绵羊心肌梗死的血管动脉生成。鉴于动物模型的高度翻译性质和杆状病毒载体的良好生物安全性,该策略可能对缺血性心脏病患者有用。
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引用次数: 0
Core role of H19 LncRNA in gastric cancer: From tumor ecosystem reprogramming to precision therapy H19 LncRNA在胃癌中的核心作用:从肿瘤生态系统重编程到精准治疗
IF 2.4 3区 生物学 Q2 GENETICS & HEREDITY Pub Date : 2026-01-15 Epub Date: 2025-11-05 DOI: 10.1016/j.gene.2025.149871
Binbin Zeng , Jianing Zhu , Yaping Wang , Chen Gu , Wenxu Zhu , Qingqing Xu , Yuxuan Wu , Juping Chen , Yang Ai , Tianyu Zhou , Ying Lin , Lixin Hua , Yayun Qian
Gastric cancer (GC) is the fifth most common malignancy and the fourth leading cause of cancer-related death worldwide. Owing to its insidious onset, most patients are diagnosed at advanced stages, marked by high recurrence, frequent metastasis, and multidrug resistance, resulting in poor outcomes. Optimizing therapeutic strategies therefore remains an urgent priority. Increasing evidence links GC initiation and progression to dysregulated expression of both coding and non-coding genes. Among them, long non-coding RNAs (lncRNAs) which recognized as pivotal regulators of gene expression have emerged as promising biomarkers and therapeutic targets. This review focuses on the lncRNA H19, highlighting its role as a central molecular hub in gastric tumor progression. H19 modulates the tumor microenvironment, promotes invasion and metastasis, reprograms cellular metabolism, and contributes to therapeutic resistance. By integrating molecular, cellular, and clinical perspectives, we provide a refined understanding of H19-driven gastric tumorigenesis and underscore its potential as a biomarker and therapeutic target. These insights offer new opportunities for early diagnosis, personalized treatment, and the development of RNA-targeted therapies for gastric cancer.
胃癌(GC)是世界上第五大最常见的恶性肿瘤,也是第四大癌症相关死亡原因。由于其发病隐匿,大多数患者诊断为晚期,特点是高复发,频繁转移和多药耐药,导致预后差。因此,优化治疗策略仍然是当务之急。越来越多的证据表明GC的发生和发展与编码和非编码基因的表达失调有关。其中,长链非编码rna (lncRNAs)被认为是基因表达的关键调控因子,已成为有希望的生物标志物和治疗靶点。这篇综述的重点是lncRNA H19,强调其在胃肿瘤进展中的中心分子枢纽作用。H19调节肿瘤微环境,促进侵袭和转移,重编程细胞代谢,并有助于治疗耐药。通过整合分子、细胞和临床观点,我们提供了对h19驱动的胃肿瘤发生的精细理解,并强调了其作为生物标志物和治疗靶点的潜力。这些见解为胃癌的早期诊断、个性化治疗和rna靶向治疗的发展提供了新的机会。
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