RNA BiologyPub Date : 2025-12-01Epub Date: 2025-03-02DOI: 10.1080/15476286.2025.2472448
Nils Peiter, Anna Einert, Pauline Just, Frida Jannasch, Marija Najdovska, Michael Rother
{"title":"Defining the methanogenic SECIS element <i>in vivo</i> by targeted mutagenesis.","authors":"Nils Peiter, Anna Einert, Pauline Just, Frida Jannasch, Marija Najdovska, Michael Rother","doi":"10.1080/15476286.2025.2472448","DOIUrl":"10.1080/15476286.2025.2472448","url":null,"abstract":"<p><p>In all domains of life, Archaea, Eukarya and Bacteria, the unusual amino acid selenocysteine (Sec) is co-translationally incorporated into proteins by recoding a UGA stop codon to a sense codon. A secondary structure on the mRNA, the selenocysteine insertion sequence (SECIS), is required, but its position, secondary structure and binding partner(s) are not conserved across the tree of life. Thus far, the nature of archaeal SECIS elements has been derived mainly from sequence analyses. A recently developed <i>in vivo</i> reporter system was used to study the structure-function relationships of SECIS elements in <i>Methanococcus maripaludis</i>. Through targeted mutagenesis, we defined the minimal functional SECIS element, the parts of the SECIS where structure and not the identity of the bases are relevant for function, and identified two conserved -and invariant- adenines that are most likely to interact with the other factor(s) of the Sec recoding machinery. Finally, we demonstrated the functionality of SECIS elements in the 5`-untranslated region of the mRNA and identified a potential mechanism of SECIS repositioning in the vicinity of the UGA for efficient selenocysteine insertion.</p>","PeriodicalId":21351,"journal":{"name":"RNA Biology","volume":" ","pages":"1-13"},"PeriodicalIF":3.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143503658","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}
EpigeneticsPub Date : 2025-12-01Epub Date: 2025-02-20DOI: 10.1080/15592294.2025.2469205
Lisha Lin, Wei Zhao, Zheng Li, Scott M Ratliff, Yi Zhe Wang, Colter Mitchell, Jessica D Faul, Sharon L R Kardia, Kira S Birditt, Jennifer A Smith
{"title":"Poly-epigenetic scores for cardiometabolic risk factors interact with demographic factors and health behaviors in older US Adults.","authors":"Lisha Lin, Wei Zhao, Zheng Li, Scott M Ratliff, Yi Zhe Wang, Colter Mitchell, Jessica D Faul, Sharon L R Kardia, Kira S Birditt, Jennifer A Smith","doi":"10.1080/15592294.2025.2469205","DOIUrl":"10.1080/15592294.2025.2469205","url":null,"abstract":"<p><p>Poly-epigenetic scores (PEGS) are surrogate measures that help capture individual-level risk. Understanding how the associations between PEGS and cardiometabolic risk factors vary by demographics and health behaviors is crucial for lowering the burden of cardiometabolic diseases. We used results from established epigenome-wide association studies to construct trait-specific PEGS from whole blood DNA methylation for systolic and diastolic blood pressure (SBP, DBP), body mass index (BMI), C-reactive protein (CRP), high- and low-density lipoprotein cholesterol (HDL-C, LDL-C), triglycerides (TG), and fasting glucose. Overall and race-stratified associations between PEGS and corresponding traits were examined in adults >50 years from the Health and Retirement Study (<i>n</i> = 3,996, mean age = 79.5 years). We investigated how demographics (age, sex, educational attainment) and health behaviors (smoking, alcohol consumption, physical activity) modified these associations. All PEGS were positively associated with their corresponding cardiometabolic traits (<i>p</i> < 0.05), and most associations persisted across all racial/ethnic groups. Associations for BMI, HDL-C, and TG were stronger in younger participants, and BMI and HDL-C associations were stronger in females. The CRP association was stronger among those with a high school degree. Finally, the HDL-C association was stronger among current smokers. These findings support PEGS as robust surrogate measures and suggest the associations may differ among subgroups.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2469205"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11844928/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143457339","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":"Coupling mechanisms coordinating mRNA translation with stages of the mRNA lifecycle.","authors":"Valeria Famà, Lucia Coscujuela Tarrero, Roberto Albanese, Lorenzo Calviello, Stefano Biffo, Mattia Pelizzola, Mattia Furlan","doi":"10.1080/15476286.2025.2483001","DOIUrl":"10.1080/15476286.2025.2483001","url":null,"abstract":"<p><p>Gene expression involves a series of consequential processes, beginning with mRNA synthesis and culminating in translation. Traditionally studied as a linear sequence of events, recent findings challenge this perspective, revealing coupling mechanisms that coordinate key steps of gene expression, even when spatially and temporally distant. In this review, we focus on translation, the final stage of gene expression, and examine its coupling with key stages of mRNA metabolism: synthesis, processing, export, and decay. For each of these processes, we provide an overview of known instances of coupling with translation. Furthermore, we discuss the role of high-throughput technologies in uncovering these intricate interactions on a genome-wide scale. Finally, we highlight key challenges and propose future directions to advance our understanding of how coupling mechanisms orchestrate robust and adaptable gene expression programs.</p>","PeriodicalId":21351,"journal":{"name":"RNA Biology","volume":" ","pages":"1-12"},"PeriodicalIF":3.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11934187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670922","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}
RNA BiologyPub Date : 2025-12-01Epub Date: 2025-04-29DOI: 10.1080/15476286.2025.2498203
Rita Pancsa, Dmitry E Andreev, Kellie Dean
{"title":"The implication of non-AUG-initiated N-terminally extended proteoforms in cancer.","authors":"Rita Pancsa, Dmitry E Andreev, Kellie Dean","doi":"10.1080/15476286.2025.2498203","DOIUrl":"https://doi.org/10.1080/15476286.2025.2498203","url":null,"abstract":"<p><p>Dysregulated translation is a hallmark of cancer, and recent genome-wide studies in tumour cells have uncovered widespread translation of non-canonical reading frames that often initiate at non-AUG codons. If an upstream non-canonical start site is located within a frame with an annotated coding sequence (CDS), such translation events can lead to the production of proteoforms with altered N-termini (PANTs). Certain examples of PANTs from oncogenes (e.g. c-MYC) and tumour suppressors (e.g. PTEN) have been previously linked to cancer. We have performed a systematic computational analysis on recently identified non-AUG initiation-derived N-terminal extensions of cancer-associated proteins, and we discuss how these extended proteoforms may acquire new oncogenic properties. We identified a loss of stability for the N-terminally extended proteoforms of oncogenes TCF-4 and SOX2. Furthermore, we discovered likely functional short linear motifs within the N-terminal extensions of oncogenes and tumour suppressors (SOX2, SUFU, SFPQ, TOP1 and SPEN/SHARP) that could provide an explanation for previously described functionalities or interactions of the proteins. In all, we identify novel cases where PANTs likely show different localization, functions, partner binding or turnover rates compared to the annotated proteoforms. Therefore, we propose that alterations in the stringency of translation initiation, often seen under conditions of cellular stress, may result in reprogramming of translation to generate novel PANTs that influence cancer progression.</p>","PeriodicalId":21351,"journal":{"name":"RNA Biology","volume":"22 1","pages":"1-18"},"PeriodicalIF":3.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12045569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144051237","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}
Redox ReportPub Date : 2025-12-01Epub Date: 2025-04-20DOI: 10.1080/13510002.2025.2491318
Nashwa Elshaer, Ahmed M Eldeeb, Ahmed A A Aioub, Ahmed S Hashem, Soumya Ghosh, Lamya Ahmed Alkeridis, Mohammed Ali Alshehri, Mustafa Shukry, Daklallah A Almalki, Hind A Alkhatabi, Mohamed Afifi, Ammar Al-Farga, Mohamed A Hendawy, Ahmed E A El-Sobki
{"title":"Zinc nanoparticles mitigate azoxystrobin and its nanoencapsulation-induced hepatic and renal toxicity in rats.","authors":"Nashwa Elshaer, Ahmed M Eldeeb, Ahmed A A Aioub, Ahmed S Hashem, Soumya Ghosh, Lamya Ahmed Alkeridis, Mohammed Ali Alshehri, Mustafa Shukry, Daklallah A Almalki, Hind A Alkhatabi, Mohamed Afifi, Ammar Al-Farga, Mohamed A Hendawy, Ahmed E A El-Sobki","doi":"10.1080/13510002.2025.2491318","DOIUrl":"https://doi.org/10.1080/13510002.2025.2491318","url":null,"abstract":"<p><p>This study sought to ascertain if zinc nanoparticles (ZnNPs) could lessen the toxicity of azoxystrobin (AZ). This naturally occurring methoxyacrylate is one of the most often used fungicides in agriculture in male albino rats. Six sets of 60 mature male albino rats were randomly assigned: control (distilled water), Azoxystrobin formulation (AZOF), Azoxystrobin nano-formula (AZON), ZnNPs, AZOF + ZnNPs, and AZON + ZnNPs. Blood and tissues were obtained for further immunohistochemical, pathological, and biochemical examination. The results showed that exposure to AZOF and AZON significantly increased the levels of the oxidative stress indicators glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA). Additionally, AZOF significantly impacts liver function bioindicators, including aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. AZOF and AZON induced damage to the liver and kidney by disrupting vascular dilatation and causing hemorrhages, apoptosis, inflammatory lymphocytes, and necrosis. Furthermore, co-administration of ZnNPs with fungicides (AZOF and AZON) can gently enhance the alterations of oxidative stress and liver function bioindicators levels. These findings showed that ZnNPs could help male rats receiving AZ treat their histologically abnormal liver and kidney.</p>","PeriodicalId":21096,"journal":{"name":"Redox Report","volume":"30 1","pages":"2491318"},"PeriodicalIF":5.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12010655/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143996445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BioengineeredPub Date : 2025-12-01Epub Date: 2025-04-15DOI: 10.1080/21655979.2025.2491936
{"title":"Statement of Retraction: Graphene based scaffolds on bone tissue engineering.","authors":"","doi":"10.1080/21655979.2025.2491936","DOIUrl":"https://doi.org/10.1080/21655979.2025.2491936","url":null,"abstract":"","PeriodicalId":8919,"journal":{"name":"Bioengineered","volume":"16 1","pages":"2491936"},"PeriodicalIF":4.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143973738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BioengineeredPub Date : 2025-12-01Epub Date: 2025-04-23DOI: 10.1080/21655979.2025.2491949
{"title":"Statement of Retraction: miR-647 inhibits hepatocellular carcinoma cell progression by targeting protein tyrosine phosphatase receptor type F.","authors":"","doi":"10.1080/21655979.2025.2491949","DOIUrl":"https://doi.org/10.1080/21655979.2025.2491949","url":null,"abstract":"","PeriodicalId":8919,"journal":{"name":"Bioengineered","volume":"16 1","pages":"2491949"},"PeriodicalIF":4.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12026219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143962772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
EpigeneticsPub Date : 2025-12-01Epub Date: 2025-04-16DOI: 10.1080/15592294.2025.2491316
Susmita Roy, Dikshita Deka, Suresh Babu Kondaveeti, Pavithra Ayyadurai, Sravani Siripragada, Neha Philip, Surajit Pathak, Asim K Duttaroy, Antara Banerjee
{"title":"An overview of potential of natural compounds to regulate epigenetic modifications in colorectal cancer: a recent update.","authors":"Susmita Roy, Dikshita Deka, Suresh Babu Kondaveeti, Pavithra Ayyadurai, Sravani Siripragada, Neha Philip, Surajit Pathak, Asim K Duttaroy, Antara Banerjee","doi":"10.1080/15592294.2025.2491316","DOIUrl":"https://doi.org/10.1080/15592294.2025.2491316","url":null,"abstract":"<p><p>Colorectal cancer (CRC) remains an alarming global health concern despite advancements in treatment modalities over recent decades. Among the various factors contributing to CRC, this review emphasizes the critical role of epigenetic mechanisms in its pathogenesis and progression. This review also describes the potential role of natural compounds in altering the epigenetic landscape, focused mainly on DNA methylation, histone modification, and non-coding RNAs. Publications from the previous five years were searched and retrieved using well-known search engines and databases like PubMed, Google Scholar, and ScienceDirect. Keywords like CRC/colorectal cancer, CAC/Colitis associated CRC, inflammasomes, epigenetic modulation, genistein, curcumin, quercetin, resveratrol, anthocyanins, sulforaphane, and epigallocatechin-3-gallate were used in various combinations during the search. These natural compounds predominantly affect pathways such as Wnt/β-catenin, NF-κB, and PI3K/AKT to suppress CRC cell proliferation and oxidative stress and enhance anti-inflammation and apoptosis. However, their clinical use is restricted due to their low bioavailability. However, multiple methods exist to overcome challenges like this, including but not limited to structural modifications, nanoparticle encapsulations, bio-enhancers, and novel advanced delivery systems. These methods improve their potential as supportive therapies that target CRC progression epigenetically with fewer side effects. Current research focuses on enhancing epigenetic targeting to control CRC progression while minimizing side effects, emphasizing improved specificity, bioavailability, and efficacy as standalone or synergistic therapies.</p>","PeriodicalId":11767,"journal":{"name":"Epigenetics","volume":"20 1","pages":"2491316"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12005453/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143986001","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":"Atoh8 expression inhibition promoted osteogenic differentiation of ADSCs and inhibited cell proliferation in vitro and rat bone defect models.","authors":"Zian Yi, Shuang Song, Yuxin Bai, Guanhua Zhang, Yuxi Wang, Zijun Chen, Xuefeng Chen, Banglian Deng, Xiangdong Liu, Zuolin Jin","doi":"10.1080/21623945.2025.2494089","DOIUrl":"10.1080/21623945.2025.2494089","url":null,"abstract":"<p><p>Stem cell-based bone tissue engineering offers a promising approach for treating oral and cranio-maxillofacial bone defects. This study investigated the role of Atoh8, a key regulator in various cells, in the osteogenic potential of adipose-derived stem cells (ADSCs). ADSCs transfected with small interfering RNA (siRNA) targeting Atoh8 were evaluated for proliferation, migration, adhesion, and osteogenic capacity. In vivo, 20 SD rats were used to assess bone regeneration using Atoh8-knockdown ADSC sheets, with new bone formation quantified via micro-CT and histological analysis. Atoh8 knockdown in vitro reduced ADSC proliferation and migration but enhanced osteogenic differentiation and upregulation of osteogenic-related factors. This approach improved bone healing in rat defect models, accelerating repair both in vitro and in vivo. The findings underscore the clinical potential of ADSCs in bone tissue engineering and elucidate Atoh8's regulatory role in ADSC osteogenesis, providing a novel therapeutic strategy for enhancing bone regeneration through targeted modulation of stem cell differentiation pathways.</p>","PeriodicalId":7226,"journal":{"name":"Adipocyte","volume":"14 1","pages":"2494089"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12077435/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143961412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}