Danni Xu , Yu Fu , Huamao Sun , Yanda Lu , Bo Shen , Xinbao Hao
{"title":"ALYREF通过依赖m5C修饰稳定了悄悄mRNA,加速鼻咽癌的发展。","authors":"Danni Xu , Yu Fu , Huamao Sun , Yanda Lu , Bo Shen , Xinbao Hao","doi":"10.1016/j.yexcr.2025.114747","DOIUrl":null,"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":3.5000,"publicationDate":"2025-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"ALYREF stabilizes CREPT mRNA to accelerate the development of nasopharyngeal carcinoma through dependence on m5C modification\",\"authors\":\"Danni Xu , Yu Fu , Huamao Sun , Yanda Lu , Bo Shen , Xinbao Hao\",\"doi\":\"10.1016/j.yexcr.2025.114747\",\"DOIUrl\":null,\"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\":3.5000,\"publicationDate\":\"2025-09-07\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Experimental cell research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0014482725003477\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental cell research","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0014482725003477","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
ALYREF stabilizes CREPT mRNA to accelerate the development of nasopharyngeal carcinoma through dependence on m5C modification
Background
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.
Methods
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.
Results
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.
Conclusion
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.
期刊介绍:
Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.