Experimental cell research最新文献

{"title":"KHSRP protects colorectal cancer cells against ferroptosis by regulating GPX4 expression through interaction with hnRNPM","authors":"Xia Ding ,&nbsp;Ningjing Zhang ,&nbsp;Shuai Zhan ,&nbsp;Wanjing Ding","doi":"10.1016/j.yexcr.2025.114812","DOIUrl":"10.1016/j.yexcr.2025.114812","url":null,"abstract":"<div><div>Ferroptosis is an iron-dependent form of programmed cell death driven by the accumulation of lipid peroxides. KHSRP, an RNA-binding protein, is known to orchestrate diverse cellular processes, including cell differentiation, proliferation, and lipid metabolism. However, its potential role in modulating ferroptosis in cancer remains unclear. In this study, we found that elevated KHSRP expression was associated with poor prognosis in colorectal cancer (CRC) patients. Knockdown of KHSRP significantly elevated lipid peroxidation, increased malondialdehyde (MDA) accumulation, and reduced glutathione (GSH) levels, ultimately triggering ferroptosis in CRC cells. Mechanistically, we discovered that KHSRP interacts with the splicing factor hnRNPM, which directly binds to GPX4 mRNA. Critically, hnRNPM overexpression effectively rescued the decrease in GPX4 expression and the ferroptotic phenotype induced by KHSRP knockdown. These results suggest that the KHSRP-hnRNPM complex binds to GPX4 mRNA and acts as a key regulator of its post-transcriptional fate to sustain GPX4 expression. Overall, our results uncover a novel regulatory mechanism whereby high KHSRP expression protects CRC cells from ferroptosis. Targeting the KHSRP–hnRNPM-GPX4 axis to overcome ferroptosis resistance represents a promising therapeutic strategy for CRC.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"453 2","pages":"Article 114812"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145426534","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":"tsRNA-10105-enriched migrasomes mediate hepatocellular carcinoma immunosuppressive microenvironment by inducing M2 Macrophage polarization","authors":"Limin Pan ,&nbsp;Ruiyao Zhou ,&nbsp;Zhikai Wen ,&nbsp;Yue Lin ,&nbsp;Huixin Cai ,&nbsp;Chengyi Lin ,&nbsp;Xuelong Xu ,&nbsp;Limin Ruan ,&nbsp;Yu Zeng ,&nbsp;Haifeng Zhang ,&nbsp;Yu Zhou ,&nbsp;Xiao Hu","doi":"10.1016/j.yexcr.2025.114729","DOIUrl":"10.1016/j.yexcr.2025.114729","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC) is characterized by a complex immunosuppressive microenvironment, which significantly influences tumor progression. Migrasomes, newly identified extracellular vesicles, have emerged as a novel mode of intercellular communication. However, their roles in HCC immune microenvironment are rarely studied. Here, we observed migrasome markers and M2 polarization levels in HCC patient tissues using immunofluorescence. Migrasomes were isolated from HCC cells and characterized using electron microscopy, immunofluorescence, and Western blot. The effects of migrasomes on macrophage polarization and HCC progression were investigated <em>in</em> <em>vitro</em> and <em>in</em> <em>vivo</em>. Small RNA-seq was conducted to screen for key tsRNA. We discovered that the levels of the migrasome marker and M2 macrophage marker were elevated in liver tumor tissues. Migrasomes derived from HepG2 induced macrophage M2 polarization, as indicated by the increased expression of M2 polarization marker, and the suppressed expression of M1 polarization marker. Macrophages treated with these migrasomes further stimulated the proliferation, migration, and invasion of malignant cells <em>in</em> <em>vitro</em> and augmented tumor growth and metastasis <em>in</em> <em>vivo</em>. Compared to the healthy individuals, the sera of HCC patients demonstrated elevated expression of tsRNA-10105 in migrasomes. Inhibition of tsRNA-10105 significantly abolished the inducing effect of cancer cell migrasomes on the M2 macrophages polarization. Our findings indicate that migrasome-derived tsRNA-10105 from HCC cells can induce the M2 macrophages polarization, which in turn augments survival and migration of HCC cells. This work provides insights into the mechanisms of the immunosuppressive microenvironment in HCC and offers novel perspectives for the immunotherapy of HCC.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"453 2","pages":"Article 114729"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000057","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":"Modelling CubAm function and regulation in proximal tubular cells using iPSC-derived kidney organoids","authors":"Carmen Llorens-Cebrià ,&nbsp;Daphne Bouwens ,&nbsp;Max Van Der Velde ,&nbsp;Mónica Duran ,&nbsp;Mireia Salvadó-Pau ,&nbsp;Irene Martínez-Díaz ,&nbsp;Jordi Vilardell-Vilà ,&nbsp;Anna Meseguer ,&nbsp;Rafael Kramann ,&nbsp;Roser Ferrer-Costa ,&nbsp;Maria José Soler ,&nbsp;Joan López-Hellín ,&nbsp;Gerard Cantero-Recasens ,&nbsp;Jitske Jansen ,&nbsp;Conxita Jacobs-Cachá","doi":"10.1016/j.yexcr.2025.114814","DOIUrl":"10.1016/j.yexcr.2025.114814","url":null,"abstract":"<div><div>Idiopathic nephrotic syndrome (INS) associated to focal segmental glomeruloesclerosis or minimal change disease is characterized by the presence of heavy levels of proteinuria. Filtrated proteins are normally actively reabsorbed in the proximal tubule by the megalin-cubilin-amnionless complex, located at the apical membrane of the proximal tubule epithelial cells. Megalin has a transmembrane domain but cubilin needs to interact with amnionless to reach the cell membrane in a complex known as CubAm. While megalin has a wide variety of ligands only a few proteins are exclusively transported by binding CubAm; one of those is Apolipoprotein A-I (ApoA-I). The reabsorption of Apolipoprotein A-I (ApoA-I) seems to be impaired in INS but this aspect of INS is difficult to study due to the low expression of CubAm in cultured proximal tubular cells as well as in other <em>in vitro</em> tubular modelling approaches. Here we show that RPTEC/TERT-1 cells cultured in monolayer barely express cubilin and amnionless proteins. In contrast, proximal tubular cells of induced Pluripotent Stem Cells (iPSCs)-derived kidney organoids showed robust expression of CubAm. In addition, protein overload induced an increase of the number of proximal tubular cells expressing cubilin that is reversed when the stimuli is removed. Finally, exogenously added ApoA-I targets cubilin suggesting that the CubAm complex is functional in our iPSCs-derived kidney organoids. Thus, kidney organoids provide a valuable system for modelling specific aspects of INS, including the impact of protein overload on tubular cells and the CubAm-mediated endocytosis of ApoA-I, which is thought to be impaired in these conditions.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"453 2","pages":"Article 114814"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145450909","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":"Developmental delay in DCP2l(3)tb of Drosophila melanogaster is due to disruption in the regulation of ecdysone signaling","authors":"Govind R. Chaudhary,&nbsp;Vaishali Yadav,&nbsp;Jagat Kumar Roy","doi":"10.1016/j.yexcr.2025.114808","DOIUrl":"10.1016/j.yexcr.2025.114808","url":null,"abstract":"<div><div>The balance between mRNA synthesis and degradation plays an important role in gene regulation, their perturbation can lead to deleterious consequences to the cell. In eukaryotes, mRNA is degraded by a decapping protein-2 (DCP2). A hypomorph mutant allele of DCP2, <em>DCP2</em>^{<em>l(3)tb</em>}, identified in our lab, shows delayed moulting, pupariation and absolute lethality in pupal stages. In <em>Drosophila</em>, moulting and pupariation are primarily regulated by ecdysone which is modulated by a few regulators synthesized by the larval brain, some are stimulatory such as Prothoracicotropic hormone (PTTH) and <em>Drosophila</em> insulin-like peptides (Dilps); whereas some are inhibitory, such as Lgr3-expressing neurons. We aimed to investigate the cause of the delay in moulting and pupariation in <em>DCP2</em>^{<em>l(3)tb</em>} homozygous mutants. Through our RNA Seq data, we found downregulated expression of brain-derived neuropeptides such as <em>PTTH</em> and <em>Dilps</em> which were further confirmed and validated through qRT-PCR and semiquantitative PCR. Furthermore, we assessed the mRNA level of <em>Lgr3</em> which was found to be upregulated in the larval CNS of <em>DCP2</em>^{<em>l(3)tb</em>} homozygotes suggesting insufficient production of stimulatory modulators. Further, providing 20H-ecdysone exogenously through diet, curtailed the extended larval life. We propose that the larval CNS of <em>DCP2</em>^{<em>l(3)tb</em>} homozygotes produces insufficient brain-derived neuropeptides to stimulate the prothoracic gland to synthesize the ecdysone required for moulting and metamorphosis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"453 2","pages":"Article 114808"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145367741","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":"The role and mechanism of fatty acid-binding protein 7 in spinal reactive astrocytes in prolonged postoperative pain induced by high-fat diet","authors":"Han Zheng ,&nbsp;Xiao Zhang ,&nbsp;Mei Li ,&nbsp;Yu Wang ,&nbsp;Shufen Guo ,&nbsp;Ming Jiang ,&nbsp;Rui Xu ,&nbsp;Yulin Huang ,&nbsp;Zhengliang Ma","doi":"10.1016/j.yexcr.2025.114801","DOIUrl":"10.1016/j.yexcr.2025.114801","url":null,"abstract":"<div><div>Obesity markedly exacerbates nociceptive sensitivity and substantially compromises the quality of life of affected people. Astrocytes orchestrate metabolic regulation and homeostatic maintenance in the central nervous system. Notably, fatty acid binding protein 7 (FABP7) is highly expressed in astrocytes that governs intracellular fatty acid uptake and transport. While systemic hyperlipidemia is pathognomonic of obesity, the mechanistic contribution of FABP7 in astrocytes to obesity-associated pain pathophysiology remains poorly characterized. The present study established a model of high-fat diet (HFD)-induced obesity combined with a standardized hind paw surgical incision paradigm, aiming to unveil the role of astrocytic FABP7 in HFD-induced chronic pain. Furthermore, an <em>in vitro</em> high-fat environment was induced by palmitic acid (PA),aiming to investigate the molecular mechanisms by which primary astrocytes were activated into the A1 phenotype to mediate neuroinflammation. FABP7 was overexpressed in the spinal dorsal of HFD mice. The activation of A1-type astrocytes and neuroinflammation cascades involving elevated iNOS eventually resulted in mechanical allodynia in HFD mice. Pharmacological inhibition of FABP7 <em>via</em> an intraperitoneal administration of SBFI-26 (20 mg/kg) significantly attenuated the paw withdrawal mechanical threshold and inhibited the A1-type astrocytes activation. PA-induced high-fat conditions promoted lipid droplet accumulation and upregulated FABP7 in astrocytes. Pharmacological inhibition of FABP7 using SBFI-26 (100 μmol/L) significantly suppressed the neurotoxic C3-positive A1 astrocyte phenotype, reduced intracellular lipid droplet accumulation, thereby inhibiting the activation of A1-type astrocytes and alleviating neuroinflammation. Overall, FABP7-mediated astrocytic reprogramming was a critical nexus bridging obesity with chronic pain. A1-astrocyte polarization initiated neuroinflammatory amplification, forming a feedforward loop perpetuating central sensitization. Our findings are expected to offer a viable target for metabolic pain management.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"453 2","pages":"Article 114801"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145388196","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":"Molecular mechanisms of cuproptosis in osteoarthritis: Pathways, crosstalk, and therapeutic opportunities","authors":"Yanyang Shen ,&nbsp;Mingdong Liu ,&nbsp;Benson O.A. Botchway ,&nbsp;Yong Zhang ,&nbsp;Xuehong Liu","doi":"10.1016/j.yexcr.2025.114800","DOIUrl":"10.1016/j.yexcr.2025.114800","url":null,"abstract":"<div><div>Osteoarthritis (OA), the most prevalent degenerative joint disorder worldwide, continues to impose significant personal and societal burdens due to the absence of effective disease-modifying therapies. Recent advances in metallobiology have identified cuproptosis, a copper (Cu)-dependent regulated cell death pathway, as a potential driver of OA pathogenesis. In OA, dysregulated Cu homeostasis has been linked to oxidative stress, inflammatory signalling activation, mitochondrial dysfunction, and direct chondrocyte injury. Mechanistically, Cu²⁺ overload promotes aggregation of lipoylated tricarboxylic acid (TCA) cycle enzymes and destabilisation of iron–sulfur clusters, thereby impairing mitochondrial integrity and cellular metabolism. Emerging evidence also highlights extensive crosstalk between cuproptosis and ferroptosis, mediated largely by glutathione depletion and glutathione peroxidase 4 (GPX4) dysfunction, which amplifies oxidative damage in joint tissues. This review synthesises current evidence on Cu metabolism, the regulation and function of cuproptosis-related genes (CRGs), and their roles in immune infiltration, inflammatory signalling, and cartilage degeneration in OA. We further examine the interplay between cuproptosis and ferroptosis, and critically evaluate therapeutic strategies, including Cu chelation, antioxidant reinforcement, and pathway modulation, that may offer disease-modifying potential. By integrating these mechanistic insights, we aim to define new translational opportunities for OA management and outline priority areas for future research.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"453 2","pages":"Article 114800"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145344447","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":"The BET degrader BETd-246 demonstrated significant anti-tumor efficacy in T-cell acute lymphoblastic leukemia by inhibiting TRAT1","authors":"Haixia Ge ,&nbsp;Huike Bai ,&nbsp;Juanjuan Yu ,&nbsp;Jia Cheng ,&nbsp;Zhongqin Jin ,&nbsp;Jian Pan ,&nbsp;Xue Li ,&nbsp;Chunxia Shi ,&nbsp;Yang Yang ,&nbsp;Shaoyan Hu ,&nbsp;Yanfang Tao","doi":"10.1016/j.yexcr.2025.114791","DOIUrl":"10.1016/j.yexcr.2025.114791","url":null,"abstract":"<div><div>T cell acute lymphoblastic leukemia (T-ALL) is a rare lymphoblastic leukemia characterized by T lymphocyte heterogeneity and diverse genetic abnormalities, accounting for approximately 15 % of childhood leukemias. BETd-246 serves as a tethering agent that links BETi-211 to thalidomide for the development of BET degraders. This compound has demonstrated superior efficacy in tumor treatment compared with traditional BET inhibitors. However, the anti-tumor effects and molecular mechanisms underlying the action of BETd-246 in T-ALL remain poorly understood. The aim of our study was to investigate the anti-tumor effects of BETd-246 and provide new insights into treatment strategies for T-ALL. In human T-ALL cell lines, BETd-246 induced degradation of BET proteins, particularly BRD4, at nanomolar concentrations. It effectively inhibited cell growth, disrupted the cell cycle, and promoted apoptosis in T-ALL cells in a concentration-dependent manner. The effects of BETd-246 were more pronounced than those of JQ1. <em>In vivo</em> experiments revealed that treatment with BETd-246 reduced proliferation and invasion of T-ALL cells and extended survival time in mouse models. RNA sequencing analysis indicated significant downregulation of T-cell receptor (TCR)-associated transmembrane adaptor 1 (TRAT1) expression in T-ALL cells treated with BETd-246. Knocking down TRAT1 resulted in increased growth inhibition and enhanced apoptosis within these cells. These findings suggest that TRAT1 plays a crucial role in mediating the effects of BETd-246 in T-ALL. Overall, our results indicate that BETd-246 is a promising therapeutic agent for treating this aggressive form of leukemia.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"453 2","pages":"Article 114791"},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274358","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":"Corrigendum to ‘Simvastatin inhibits the development of radioresistant esophageal cancer cells by increasing the radiosensitivity and reversing EMT process via the PTEN-PI3K/AKT pathway’ [Exp Cell Res. 2018 Jan 15;362(2):362–369]","authors":"Yingying Jin,&nbsp;Kun Xu,&nbsp;Qingjuan Chen,&nbsp;Baofeng Wang,&nbsp;Jiyuan Pan,&nbsp;Shan Huang,&nbsp;Yang Wei,&nbsp;Hongbing Ma","doi":"10.1016/j.yexcr.2025.114792","DOIUrl":"10.1016/j.yexcr.2025.114792","url":null,"abstract":"","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"453 1","pages":"Article 114792"},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145312708","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":"Maternal protein restriction promotes cardiac disorders by disrupting heart developmental morphophysiology in young male offspring rats","authors":"Lucas Sobrinho Lemos ,&nbsp;Matheus Naia Fioretto ,&nbsp;Isabelle Tenori Ribeiro ,&nbsp;Luísa Annibal Barata ,&nbsp;Flávia Alessandra Maciel ,&nbsp;Felipe Leonardo Fagundes ,&nbsp;Renato Mattos ,&nbsp;Luiz Marcos Frediani Portela ,&nbsp;João Miguel Barboza ,&nbsp;Beatriz Souza de Oliveira ,&nbsp;Keila Emílio de Almeida ,&nbsp;Sérgio Alexandre Alcantara dos Santos ,&nbsp;Clélia Akiko Hiruma Lima ,&nbsp;José Ricardo de Arruda Miranda ,&nbsp;Elena Zambrano ,&nbsp;Luis Antonio Justulin","doi":"10.1016/j.yexcr.2025.114795","DOIUrl":"10.1016/j.yexcr.2025.114795","url":null,"abstract":"<div><div>In recent years, cardiovascular diseases have been one of the leading causes of death worldwide. Epidemiological and experimental studies have linked adverse intrauterine conditions with an susceptibility to cardiovascular and metabolic diseases in subsequent generations, a concept related to the Developmental Origins of Health and Disease (DOHaD). Here, we evaluated the maternal protein restriction (MPR), and its harmful effects on the cardiac morphophysiology of offspring in early life. During gestation and lactation, the pregnant rats were divided into two groups: Control (CTR), which received a normoprotein diet (17 % protein), and Gestational and Lactational Low-Protein (GLLP), which received a hypoprotein diet (6 % protein). At postnatal day 21, the offspring were euthanized. There was a decrease in serum levels of IGF1, an increase in testosterone, and a decrease in several phenotypic parameters in the heart, such as the size of cardiomyocytes and their nuclei, collagen, reticular and elastic fibers, and mast cells in the GLLP group. We observed that MPR led to electrical disorders in the heart (bradycardia), in addition to impacting angiogenic proteins (high Aquaporin1 and PECAM-1), and proteins associated with the antioxidant system (low Peroxiredoxin 4 and high GSTpi expressions) in the GLLP group. These adverse effects early in life increase the risk of pathophysiological remodeling of the heart, with the potential for hypertension, hypertrophy, and cardiovascular disease later in life.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"453 1","pages":"Article 114795"},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145312715","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":"Epitranscriptomic analysis reveals features of NAD-capped RNAs upon supplementation of nicotinamide mononucleotide in human","authors":"Shuwen Ge ,&nbsp;Yandong Liu ,&nbsp;Dean Li ,&nbsp;Guojing Han ,&nbsp;Kongyan Niu ,&nbsp;Hujun Ju ,&nbsp;Hao Zhou ,&nbsp;Rui Liu ,&nbsp;Zhengjiang Zhu ,&nbsp;Nan Liu ,&nbsp;Lefeng Qu","doi":"10.1016/j.yexcr.2025.114780","DOIUrl":"10.1016/j.yexcr.2025.114780","url":null,"abstract":"<div><div>Nicotinamide mononucleotide (NMN), a precursory metabolite of NAD, has been demonstrated to boost cellular NAD level that is coupled with various age-related beneficial effects in animal models. NAD-capped RNA (NAD-RNA) represents a critical but poorly studied modification at the epitranscriptomic level. Here we examine the impact of NMN supplementation on NAD-RNA in human peripheral blood mononuclear cells (PBMCs). We demonstrated that NMN supplementation increases NAD turnover coupled with a reduction in NAD-capped RNAs in both human and dog, revealing blood-derived NAD-RNAs as potential biomarkers sensitized to NMN exposure.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"453 1","pages":"Article 114780"},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274393","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}