[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-332480-105":59,"doc-detail-332480-en":130},{"code":4,"msg":5,"data":6},0,"success",[7,13,18,23,28,33,38,43,48,51,55],{"id":8,"doc_module":4,"doc_module_name":9,"category_name":10,"show_sort_weight":11,"slug":12},1,"Document","Story & Novel",90,"story-novel",{"id":14,"doc_module":4,"doc_module_name":9,"category_name":15,"show_sort_weight":16,"slug":17},2,"Literature",80,"literature",{"id":19,"doc_module":4,"doc_module_name":9,"category_name":20,"show_sort_weight":21,"slug":22},4,"Exam",70,"exam",{"id":24,"doc_module":4,"doc_module_name":9,"category_name":25,"show_sort_weight":26,"slug":27},5,"Comic",60,"comic",{"id":29,"doc_module":4,"doc_module_name":9,"category_name":30,"show_sort_weight":31,"slug":32},6,"Technology",50,"technology",{"id":34,"doc_module":4,"doc_module_name":9,"category_name":35,"show_sort_weight":36,"slug":37},7,"Healthcare",40,"healthcare",{"id":39,"doc_module":4,"doc_module_name":9,"category_name":40,"show_sort_weight":41,"slug":42},8,"Research & Report",30,"research-report",{"id":44,"doc_module":4,"doc_module_name":9,"category_name":45,"show_sort_weight":46,"slug":47},9,"Religion & Spirituality",20,"religion-spirituality",{"id":46,"doc_module":4,"doc_module_name":9,"category_name":49,"show_sort_weight":46,"slug":50},"World Cup","world-cup",{"id":52,"doc_module":4,"doc_module_name":9,"category_name":53,"show_sort_weight":52,"slug":54},10,"Lifestyle","lifestyle",{"id":56,"doc_module":4,"doc_module_name":9,"category_name":57,"show_sort_weight":24,"slug":58},19,"General","general",{"code":4,"msg":60,"data":61},"ok",{"site_id":62,"language":63,"slug":64,"title":65,"keywords":66,"description":67,"schema_data":68,"social_meta":123,"head_meta":125,"extra_data":127,"updated_unix":129},105,"en","prmt5-mediated-fubp1-methylation-accelerates-prostate-cancer-progression","PRMT5-mediated FUBP1 methylation accelerates prostate cancer progression","","Strategies beyond hormone-related therapy are needed to improve prostate cancer outcomes. The study shows that FUBP1 and its methylation are essential for prostate cancer progression, and that a competitive peptide interfering with FUBP1 methylation suppresses disease development. FUBP1 accelerates tumor growth across multiple preclinical models. PRMT5-mediated FUBP1 methylation, regulated by BRD4, is critical for oncogenic effects and correlates with earlier biochemical recurrence in patient data.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/prmt5-mediated-fubp1-methylation-accelerates-prostate-cancer-progression/332480/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/prmt5-mediated-fubp1-methylation-accelerates-prostate-cancer-progression/332480.png","ImageObject",300,407,{"name":92,"@type":93},"Levi","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-11-04","2026-09-21",true,{"@type":102,"interactionType":103,"userInteractionCount":19},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What is the central finding about PRMT5-mediated FUBP1 methylation?","Question",{"text":112,"@type":113},"PRMT5-mediated methylation of FUBP1 is crucial for prostate cancer progression and oncogenic effects. It also relates to earlier biochemical recurrence in the patient cohort.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How does the study test therapeutic potential?",{"text":117,"@type":113},"It uses a competitive peptide that disrupts the interaction between FUBP1 and PRMT5. Delivered via nanocomplexes, the peptide blocks FUBP1 methylation and inhibits prostate cancer development in preclinical models.",{"name":119,"@type":110,"acceptedAnswer":120},"Why is FUBP1 considered important in prostate cancer progression?",{"text":121,"@type":113},"FUBP1 is shown to be essential for progression and to accelerate development across various preclinical models. Genetic mouse models expressing FUBP1 mutants deficient in PRMT5-mediated methylation show suppressed progression.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},332480,1792204600,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":19,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145,"preview_page_count":4},7971461740909,"https://ap-avatar.wpscdn.com/davatar_155a257f0dc6eb9ab79c44ca47cae57d","The Journal of Clinical Investigation RESEAR CH ARTICLE  \nPRMT5-mediated FUBP1 methylation accelerates prostate cancer progression  \nWeiwei Yan,1 Xun Liu,2 Xuefeng Qiu,3 Xuebin Zhang,1 Jiahui Chen,1 Kai Xiao,1 Ping Wu,4 Chao Peng,4 Xiaolin Hu,5  \nZengming Wang,6 Jun Qin,6 Liming Sun,1 Luonan Chen,1 Denglong Wu,7 Shengsong Huang,7 Lichen Yin,2 and Zhenfei Li1,7,8  \n1Key Laboratory of Multi-Cell Systems, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China. 2Institute of Functional Nano and Soft Materials (FUNSOM), Jiangsu Key Laboratory for Carbon-Based Functional Materials and Devices, Collaborative Innovation Center of Suzhou Nano Science and Technology, Soochow University, Suzhou, China. 3Department of Urology, Drum Tower Hospital, Medical School of Nanjing University, Institute of Urology, Nanjing University, Nanjing, China. 4National Facility for Protein Science Shanghai, Shanghai Advanced Research Institute, Chinese Academy of Sciences, Shanghai, China. 5State Key Laboratory of Systems Medicine for Cancer, Center for Single-Cell Omics, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China. 6CAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China. 7Department of Urology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China. 8Key Laboratory of Systems Health Science of Zhejiang Province, School of Life Science, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou, China.  \nStrategies beyond hormone-related therapy need to be developed to improve prostate cancer mortality. Here, we show that FUBP1 and its methylation were essential for prostate cancer progression, and a competitive peptide interfering with FUBP1 methylation suppressed the development of prostate cancer. FUBP1 accelerated prostate cancer development in various preclinical models. PRMT5-mediated FUBP1 methylation, regulated by BRD4, was crucial for its oncogenic effect and correlated with earlier biochemical recurrence in our patient cohort. Suppressed prostate cancer progression was observed in various genetic mouse models expressing the FUBP1 mutant deficient in PRMT5-mediated methylation. A competitive peptide, which was delivered through nanocomplexes, disrupted the interaction of FUBP1 with PRMT5, blocked FUBP1 methylation, and inhibited prostate cancer development in various preclinical models. Overall, our findings suggest that targeting FUBP1 methylation provides a potential therapeutic strategy for prostate cancer management.  \nIntroduction  \nProstate cancer is a major global health care challenge (1, 2). Androgens from the testis and the adrenal gland bind to androgen receptor (AR) to activate AR signaling and facilitate prostate cancer progression (3, 4). Thus, the androgen biosynthesis pathway andAR signaling are the main therapeutic targets for prostate cancer (5–9). Hormonal therapy has been the principal treatment for decades. Although it is initially effective, patients inevitably develop treatment resistance due to increasing tumor heterogeneity (10–12) . Consequently, novel strategies beyond hormone therapy are required to improve the clinical benefits for prostate cancer patients (8, 13) .  \nTranscriptional factors are recognized as potential therapeutic targets for prostate cancer, owing to its crucial role in a myriad of physiological and pathological processes (14–16). Gaining insight into key transcriptional factors implicated in prostate cancer and developing corresponding treatments would provide innovative approaches for disease management beyond hormone-related treatment (17–19). Far-upstream element (FUSE)–binding protein 1 (FUBP1) is a versatile DNA-and RNA-binding protein i","cbCaitX5rLOfAlpD","https://ap.wps.com/l/cbCaitX5rLOfAlpD","pdf",7974583,18,"English","# Introduction\n## Prostate cancer as a therapeutic challenge\n## FUBP1 and methylation biology\n## Study objective and approach","[{\"question\":\"What is the central finding about PRMT5-mediated FUBP1 methylation?\",\"answer\":\"PRMT5-mediated methylation of FUBP1 is crucial for prostate cancer progression and oncogenic effects. It also relates to earlier biochemical recurrence in the patient cohort.\"},{\"question\":\"How does the study test therapeutic potential?\",\"answer\":\"It uses a competitive peptide that disrupts the interaction between FUBP1 and PRMT5. Delivered via nanocomplexes, the peptide blocks FUBP1 methylation and inhibits prostate cancer development in preclinical models.\"},{\"question\":\"Why is FUBP1 considered important in prostate cancer progression?\",\"answer\":\"FUBP1 is shown to be essential for progression and to accelerate development across various preclinical models. Genetic mouse models expressing FUBP1 mutants deficient in PRMT5-mediated methylation show suppressed progression.\"}]","PRMT5-mediated FUBP1 methylation accelerates prostate cancer progression | PDF",1789998409,45]