Experimental cell research最新文献

{"title":"Semaphorin7A-expressing mast cell exosomes promote wound healing","authors":"Kyung-Ah Cho ,&nbsp;Hyeon Ju Kim ,&nbsp;SeoYi Choi ,&nbsp;So-Youn Woo ,&nbsp;Joo Young Roh","doi":"10.1016/j.yexcr.2025.114771","DOIUrl":"10.1016/j.yexcr.2025.114771","url":null,"abstract":"<div><div>Emerging evidence indicates that mast cells contribute to tissue repair, in addition to their well-established roles in immunity. We previously showed the effects of conditioned medium derived from the human mast cell line HMC-1 on skin wound healing. In this study, we assessed the regenerative potential of HMC-1 exosomes in the skin wound healing process and identified the key molecules involved. HMC-1 exosomes are rich in semaphorin 7A (SEMA7A), a key regulator of extracellular matrix (ECM) remodeling, along with canonical exosomal markers. We found that HMC-1 exosomes could promote dermal fibroblast proliferation and upregulate fibronectin and collagen type I expression. Furthermore, topical application of HMC-1 exosomes accelerated wound closure and enhanced tissue regeneration in both wild-type and mast cell-deficient mice. Notably, SEMA7A-deficient HMC-1 exosomes exhibited reduced ECM synthesis in dermal fibroblasts and impaired wound healing <em>in vivo</em>, regardless of the presence of mast cells. These findings suggest that mast cell-derived exosomes can serve as promising cell-free therapeutic agents for wound repair.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 2","pages":"Article 114771"},"PeriodicalIF":3.5,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145120647","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":"Optogenetic engineered macrophages for light-induced M1 polarization and enhanced chemo-immunotherapy in melanoma models","authors":"Kunqian He ,&nbsp;Hao Jiang ,&nbsp;Wanqi Zhang ,&nbsp;Nan Yang ,&nbsp;Shuangjiang Li ,&nbsp;Yanguo Wang ,&nbsp;Junbo Zhang ,&nbsp;Xinying Li ,&nbsp;Liuchang Tan ,&nbsp;Guihong Yang ,&nbsp;Hongli Li ,&nbsp;Yuangang Lu","doi":"10.1016/j.yexcr.2025.114770","DOIUrl":"10.1016/j.yexcr.2025.114770","url":null,"abstract":"<div><div>Macrophage-based adoptive cell therapies hold promise for solid tumors, but spatiotemporally controlling macrophage polarization within the immunosuppressive tumor microenvironment remains challenging. Here, we aimed to validate an optogenetic strategy using the LOV2-STIM1 system to achieve light-induced, sustained M1 polarization of macrophages. Upon blue light stimulation, engineered macrophages robustly exhibited M1 phenotypes, suppressed melanoma cell proliferation, migration, and invasion in vitro, and recapitulated the antitumor functions of M1 macrophages. Notably, combining light-activated engineered macrophages with temozolomide in melanoma models resulted in synergistic inhibition of tumor growth. This synergy is accompanied by a profound remodeling of the tumor immune microenvironment, characterized by M1-driven reversal of chemoresistance and enhanced infiltration of cytotoxic CD8⁺ T cells. Our findings establish a proof-of-concept for optogenetic regulation of macrophage polarization and demonstrate its feasibility for enhancing antitumor effects and chemosensitivity in melanoma models, providing a promising and controllable platform for macrophage-based immunotherapy.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 2","pages":"Article 114770"},"PeriodicalIF":3.5,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137094","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":"Primary partitioning principles of the cell: Cytoophidium assembly, phase separation and membrane enclosure","authors":"Ji-Long Liu","doi":"10.1016/j.yexcr.2025.114766","DOIUrl":"10.1016/j.yexcr.2025.114766","url":null,"abstract":"<div><div>In the 4.6 billion year history, the Earth we live on has nurtured a diverse range of life forms. The basic unit of life is the cell. Since the discovery of cells 360 years ago, scientists have gained a deep understanding of their structure, function, and heterogeneity. In order to understand the mechanisms and laws of cell structure, here I propose three primary partitioning principles of the cell, namely cytoophidium assembly, phase separation, and membrane enclosure. From the perspective of partitioning principles, I introduce these three principles separately and then compare them. Furthermore, I attempt to elucidate the primary partitioning principles from the perspectives of mathematics, physics, chemistry, evolution, and communications.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 2","pages":"Article 114766"},"PeriodicalIF":3.5,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145120558","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":"Deficiency of vitamin D-binding protein exacerbates liver fibrosis by disrupting iron homeostasis via the activation of YAP signaling","authors":"Qing Zheng ,&nbsp;Qingquan Tan ,&nbsp;Dan Wang ,&nbsp;Yanling Ma ,&nbsp;Yanni Zhou ,&nbsp;Yonghua Chen ,&nbsp;Dan Long ,&nbsp;Jiayin Yang ,&nbsp;Li Feng","doi":"10.1016/j.yexcr.2025.114767","DOIUrl":"10.1016/j.yexcr.2025.114767","url":null,"abstract":"<div><div>Liver fibrosis is a chronic progressive disease that can advance to cirrhosis or hepatocellular carcinoma if untreated. While liver transplantation remains the only curative option for end-stage fibrosis, the development of alternative therapies is urgently needed. In this study, we investigated the role of vitamin D-binding protein (VDBP) in hepatic fibrosis using clinical samples and a CCl₄-induced mouse model. We observed significant downregulation of VDBP in fibrotic human and murine livers, suggesting that VDBP may serve as a potential biomarker for disease progression. VDBP knockout (VDBP-KO) mice exhibited exacerbated fibrosis, iron overload, and ferroptosis activation, accompanied by dysregulation of the Hippo-YAP pathway. In vitro, VDBP overexpression reversed these effects, while in vivo treatment with the YAP inhibitor verteporfin attenuated fibrosis, normalized iron homeostasis, and suppressed ferroptosis in VDBP-KO mice. Our findings demonstrate that VDBP plays a pivotal role in maintaining iron balance, inhibiting YAP signaling, and preventing ferroptosis during fibrogenesis. Elucidating the molecular mechanisms of VDBP and its downstream pathways may provide novel therapeutic targets for liver fibrosis. This could significantly improve the clinical management of hepatic fibrosis and offer new hope for patients suffering from this debilitating disease.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 2","pages":"Article 114767"},"PeriodicalIF":3.5,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145109897","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":"Co-delivery of ripasudil and dexamethasone in trabecular meshwork cells for potential prevention of GC-induced ocular hypertension","authors":"Tilahun Ayane Debele ,&nbsp;Yong Yuan ,&nbsp;Winston Kao ,&nbsp;Chia-Yang Liu ,&nbsp;Eskezeia Y. Dessie ,&nbsp;Yoonjee C. Park","doi":"10.1016/j.yexcr.2025.114759","DOIUrl":"10.1016/j.yexcr.2025.114759","url":null,"abstract":"<div><div>The purpose of this in vitro study is to investigate whether the co-delivery of Ripasudil (Rip) can suppress the expression of genes related to glaucoma pathogenesis induced by prolonged dexamethasone (Dex) use, which can lead to ocular hypertension and potentially glaucoma formation. The effects of Rip (10 μM) on Dex (100 nM)-treated human trabecular meshwork (TM) cells were tested through co-delivery and sequential treatments using RNA-seq. Genome-wide analysis was performed using gene ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis with Enrichr and DAVID gene analysis tools. Gene enrichment and pathway analysis revealed that Rip, when co-delivered or sequentially delivered with Dex, influenced genes involved in glaucoma-related pathways such as focal adhesion, extracellular matrix (ECM) organization, and regulation of the actin cytoskeleton. Rip treatment downregulated genes like <em>ACTA2, COL11A1, ECM2, MBP</em>, and <em>ANGPTL7</em>, which are associated with increased outflow resistance and elevated intraocular pressure (IOP). Additionally, Rip upregulated <em>ITGA11</em>, a gene that promotes actin cytoskeleton reorganization and TM cell relaxation by inhibiting the Rho-ROCK pathway. Overall, co-delivery or sequential delivery of Rip can reverse or prevent Dex-induced ocular hypertension and glaucoma formation by modulating the expression of glaucoma-related genes at the transcriptional level.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 2","pages":"Article 114759"},"PeriodicalIF":3.5,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091470","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":"USP11 stabilizes RALY to promote FXYD5-mediated aerobic glycolysis and aggravate pancreatic cancer progression","authors":"Hongmin Xie ,&nbsp;Langxia Liao ,&nbsp;Jiaxuan Li ,&nbsp;Runsheng Cai ,&nbsp;HongBiao He ,&nbsp;Min Lu","doi":"10.1016/j.yexcr.2025.114758","DOIUrl":"10.1016/j.yexcr.2025.114758","url":null,"abstract":"<div><h3>Background</h3><div>Pancreatic cancer (PC) is a highly malignant and aggressive gastrointestinal malignancy with a poor prognosis for patients. Aerobic glycolysis serves as a critical metabolic driver of PC progression. Our study aims to elucidate the mechanism by which FXYD5 regulates aerobic glycolysis in PC.</div></div><div><h3>Methods</h3><div>Cell viability was assessed using CCK-8. Cell proliferation was tested by colony formation assay. Lactic acid production and ATP levels were measured by commercial kits. Extracellular acidification rate (ECAR) was detected using the Seahorse XF96 analyzer. RNA immunoprecipitation (RIP) was employed to validate the binding of RALY to FXYD5 mRNA. The interaction between RALY and USP11, as well as the ubiquitinated level of RALY, were probed by co-immunoprecipitation (Co-IP) assay. A subcutaneous xenograft tumor model was established to verify the <em>in vitro</em> findings.</div></div><div><h3>Results</h3><div>Knockdown of FXYD5 suppressed lactic acid production, ECAR, ATP levels, and the expression of aerobic glycolysis-related key markers (GLUT1 and HK2) in PC cells. RALY directly bound to FXYD5 mRNA to promote its stability in PC cells. RALY facilitated aerobic glycolysis to increase PC tumor growth by up-regulating FXYD5 expression <em>in vitro</em> and <em>in vivo</em>. Deubiquitinating enzyme USP11 reduced the ubiquitinated level of RALY to maintain its protein stability. USP11 knockdown restrained aerobic glycolysis of PC cells, which was reversed by RALY overexpression.</div></div><div><h3>Conclusion</h3><div>USP11 stabilized FXYD5 mRNA by promoting RALY deubiquitinated modification to increase PC cell aerobic glycolysis and exacerbate tumor progression.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 2","pages":"Article 114758"},"PeriodicalIF":3.5,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091453","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":"Wings of Enlightenment: The Jiujiang International Drosophila Conference (2016–2025) – Where Alpine Curiosity Fuels Scientific Frontiers","authors":"Ji-Long Liu","doi":"10.1016/j.yexcr.2025.114756","DOIUrl":"10.1016/j.yexcr.2025.114756","url":null,"abstract":"<div><div>Amidst the mist-clad summits of Mount Lu and the cultural heartbeat of Mount Heng, the Jiujiang International <em>Drosophila</em> Conference (2016–2025) has emerged as a crucible for curiosity-driven discovery, merging ancient Chinese traditions with cutting-edge scientific exploration. Spanning four transformative editions—Jiujiang (2016, 2018, 2023), and Hengyang (2025)—the event has redefined biomedicine's intellectual terrain. Rooted in the philosophical legacy of the White Deer Grotto Academy, a UNESCO World Heritage site celebrated for its fusion of Daoist contemplation and empirical rigor, and the Stone Drum Academy, cradle of Hunan's intellectual traditions, the conference harmonises China's cultural heritage with global scientific inquiry. Featuring pioneering research on <em>Drosophila</em> models for metabolism, development, cancer, neurodegeneration, and circadian rhythms, the conference has catalysed cross-continental collaborations, proving that scientific frontiers thrive where alpine curiosity intersects with microscopic innovation.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 2","pages":"Article 114756"},"PeriodicalIF":3.5,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145085638","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":"TFAP4/DLGAP5 promotes tumor progression and macrophage M2 polarization in prostate cancer by activating the JAK2/STAT3 signaling","authors":"Sen Li,&nbsp;Qingchuan Dong,&nbsp;Wei Ren,&nbsp;Yi Sun,&nbsp;Zhigang Wang,&nbsp;Liang Pan","doi":"10.1016/j.yexcr.2025.114753","DOIUrl":"10.1016/j.yexcr.2025.114753","url":null,"abstract":"<div><h3>Background</h3><div>M2-polarized macrophages exhibit pro-tumorigenic functions in multiple malignancies, including prostate cancer (PC). Discs large homolog-associated protein 5 (DLGAP5) acts as an oncogenic driver in PC. This study aims to delineate the precise role and mechanistic basis of DLGAP5 in regulating PC-associated macrophage polarization.</div></div><div><h3>Methods</h3><div>Bioinformatics analyses were used to observe the expression profiling and polarization association of DLGAP5 and its upstream transcription factors (TFs). Cell phenotypes were assessed by measuring cell invasion, migration, apoptosis, and proliferation. After co-culture with PC cells, M2 macrophage polarization was evaluated by measuring M2-associated markers through quantitative PCR, Western blot, and flow cytometry. Xenograft tumor models were employed to validate the oncogenic role of DLGAP5 <em>in vivo</em>. Chromatin immunoprecipitation (ChIP) and luciferase reporter assays were used to confirmed the functional interaction between transcription factor AP-4 (TFAP4) and the DLGAP5 promoter.</div></div><div><h3>Results</h3><div>DLGAP5 and TFAP4 were upregulated in PC tumors and cell lines. Elevated DLGAP5 expression was significantly associated with higher Gleason score, advanced clinical stage, and worse prognosis. Depletion of DLGAP5 suppressed cell growth, migration, and invasion capacities <em>in vitro</em>. Moreover, DLGAP5 depletion attenuated the M2 polarization of PC-associated macrophages. Also, knockdown of DLGAP5 decreased tumorigenicity and macrophage M2 polarization <em>in vivo</em>. Mechanistically, TFAP4 transcriptionally activated the DLGAP5 promoter to upregulate DLGAP5 expression. Loss of TFAP4 suppressed tumor cell growth, migratory capacity, and invasiveness, as well as macrophage M2 polarization, all of which could be rescued through DLGAP5 re-expression. Additionally, TFAP4 activated the JAK2/STAT3 signaling through DLGAP5 in PC cells. Inhibition of JAK2/STAT3 signaling reversed DLGAP5-mediated malignant phenotypes and macrophage M2 polarization.</div></div><div><h3>Conclusion</h3><div>Our findings demonstrate that TFAP4-transcriptionally activated DLGAP5 drives PC progression by promoting tumorigenic properties and macrophage M2 polarization, establishing the TFAP4/DLGAP5 axis as a potential therapeutic target for PC.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 2","pages":"Article 114753"},"PeriodicalIF":3.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145080096","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":"PSPC1 knockout promotes radiosensitivity, inhibits EMT, and metastasis of nasopharyngeal carcinoma cells","authors":"Huocong He ,&nbsp;Zhengrong Huang ,&nbsp;Fuli Wen ,&nbsp;Na Ge ,&nbsp;Xiandong Lin ,&nbsp;Jianru Pan","doi":"10.1016/j.yexcr.2025.114755","DOIUrl":"10.1016/j.yexcr.2025.114755","url":null,"abstract":"<div><h3>Purpose</h3><div>Paraspeckle component 1 (PSPC1) is upregulated in numerous cancers and is associated with reduced patient survival rates. Our previous research indicated that elevated PSPC1 levels in nasopharyngeal carcinoma (NPC) are positively linked to radiation resistance and tumor metastasis, two primary clinical challenges in NPC treatment. However, the precise role of PSPC1 in radiation resistance and metastasis of NPC cells remains unclear. This study aimed to explore the molecular mechanisms by which PSPC1 influences radiation resistance and metastasis in NPC.</div></div><div><h3>Methods</h3><div>Using the radiation-resistant R743 and radiosensitive CNE2 cell lines of NPC, we examined the impact of PSPC1 expression on post-radiation survival, cell cycle progression, apoptosis, migration, invasion, and tumor growth. CRISPR/Cas9 genome editing was employed to generate PSPC1 knockout (KO) lines in R743 cells, while PSPC1 overexpression (pcD-PSPC1) was achieved in CNE2 cells via pcDNA3.1(+)-PSPC1 plasmid transfection.</div></div><div><h3>Results</h3><div>PSPC1 knockout converted R743 cells from radioresistant to radiosensitive, whereas PSPC1 overexpression decreased radiosensitivity in CNE2 cells. Cell cycle analysis revealed that PSPC1 KO arrested R743 cells in the G2/M phase post-irradiation, while PSPC1 overexpression prevented G2/M phase arrest in CNE2 cells. PSPC1 KO increased irradiation-induced apoptosis in R743 cells, whereas PSPC1 overexpression decreased it in CNE2 cells. Post-radiation, PSPC1 KO cells showed significantly reduced migration and invasion abilities. Bioinformatics analysis identified SFPQ as a PSPC1-interacting protein, with PSPC1 KO resulting in SFPQ downregulation. Additionally, PSPC1 KO enhanced the radiosensitivity of xenografted tumors in nude mice.</div></div><div><h3>Conclusion</h3><div>Our findings suggest that PSPC1 is a pivotal factor in enhancing the survival and spread of NPC cells post-radiation. Targeting PSPC1 or its downstream pathways could offer novel strategies to overcome radiation resistance and metastasis in NPC cells.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 2","pages":"Article 114755"},"PeriodicalIF":3.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145080067","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":"ALYREF stabilizes CREPT mRNA to accelerate the development of nasopharyngeal carcinoma through dependence on m5C modification","authors":"Danni Xu ,&nbsp;Yu Fu ,&nbsp;Huamao Sun ,&nbsp;Yanda Lu ,&nbsp;Bo Shen ,&nbsp;Xinbao Hao","doi":"10.1016/j.yexcr.2025.114747","DOIUrl":"10.1016/j.yexcr.2025.114747","url":null,"abstract":"<div><h3>Background</h3><div>Nasopharyngeal carcinoma (NPC) is a kind of tumor disease with high malignant degree. CREPT expression was elevated abnormally in multi-cancers. However, the role and regulatory mechanism of CREPT in NPC remains unknown.</div></div><div><h3>Methods</h3><div>NPC clinical samples, NPC cells, and nude mice served as experimental objects. The levels of molecules were detected using RT-qPCR,Western blot, IF and IHC experiments. Malignant activities of NPC cells were evaluated using CCK-8, EdU and clone formation, flow cytometry and TUNEL. Kaplan-Meier and Pearson correlation analysis were employed to analysis of the relationships between CREPT expression and prognosis/ALYREF expression in NPC patients. The interaction between ALYREF and CREPT was validated using RIP, RNA pull-down and dual luciferase experiment.</div></div><div><h3>Results</h3><div>Upregulation of CREPT and ALYREF expression was observed in NPC samples including the tissues of NPC patients and cells. CREPT knockdown reduced NPC cell viability, proliferation and enhanced NPC cell apoptosis and suppressed tumor growth through deactivating Wnt/β-catenin pathway, but the results of ALYREF overexpression had the inverse results of CREPT knockdown. Furthermore, the combination of CREPT knockdown and ALYREF overexpression compromised ALYREF overexpression-mediated the influences on NPC cells, tumor growth and motivating Wnt/β-catenin pathway. Furthermore, ALYREF interacted with CREPT mRNA and ALYREF promoted the stability of CREPT mRNA in m5C-dependent manner.</div></div><div><h3>Conclusion</h3><div>ALYREF stabilized CREPT mRNA through interacting with m5C-labeled CREPT mRNA to elevate CREPT expression, thus activating Wnt/β-catenin pathway and facilitating NPC progression.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"452 2","pages":"Article 114747"},"PeriodicalIF":3.5,"publicationDate":"2025-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029123","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}