[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-seo-374645-105":3,"detail-sidebar-cat-0-en-105":81,"doc-detail-374645-en":131},{"code":4,"msg":5,"data":6},0,"ok",{"site_id":7,"language":8,"slug":9,"title":10,"keywords":11,"description":12,"schema_data":13,"social_meta":74,"head_meta":76,"extra_data":78,"updated_unix":80},105,"en","flap-endonuclease-1-promotes-pancreatic-cancer-progression-via-aktmtor-signaling-pathway","Flap endonuclease-1 promotes pancreatic cancer progression via AKT/mTOR signaling pathway","","Pancreatic cancer remains highly lethal, and the role of flap endonuclease-1 (FEN1) in its progression is unclear. This study analyzes FEN1 expression and prognostic value using public genomic databases, then manipulates FEN1 in pancreatic cancer cell lines via lentiviral knockdown and overexpression. Cellular proliferation, migration, and invasion are tested in vitro, with tumorigenicity assessed using nude mouse xenografts. Mechanisms are investigated by RNA sequencing and validated by western blot, identifying an AKT/mTOR-driven epithelial-mesenchymal transition program.",{"@graph":14,"@context":73},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/healthcare/","Healthcare",3,{"item":32,"name":10,"@type":21,"position":33},"https://docshare.wps.com/document/flap-endonuclease-1-promotes-pancreatic-cancer-progression-via-aktmtor-signaling-pathway/374645/",4,{"url":32,"name":10,"@type":35,"image":36,"author":41,"headline":10,"publisher":44,"fileFormat":47,"inLanguage":8,"description":12,"dateModified":48,"datePublished":49,"encodingFormat":47,"isAccessibleForFree":50,"interactionStatistic":51},"DigitalDocument",{"url":37,"@type":38,"width":39,"height":40},"https://docshare.wps.com/thumbnails/flap-endonuclease-1-promotes-pancreatic-cancer-progression-via-aktmtor-signaling-pathway/374645.png","ImageObject",300,407,{"name":42,"@type":43},"Chumphorn","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-10-30","2026-09-23",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",11,{"@type":57,"mainEntity":58},"FAQPage",[59,65,69],{"name":60,"@type":61,"acceptedAnswer":62},"What is the study purpose regarding FEN1 in pancreatic cancer?","Question",{"text":63,"@type":64},"To determine the biological functions and underlying mechanisms of FEN1 during pancreatic cancer progression.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"How was FEN1 function tested in pancreatic cancer models?",{"text":68,"@type":64},"FEN1 expression and prognostic significance were analyzed using GEO, TCGA, and GTEx, and FEN1 was knocked down or overexpressed in pancreatic cancer cell lines using lentiviral vectors. Proliferation, migration, and invasion were measured in vitro, while tumor growth was evaluated in nude mouse xenografts.",{"name":70,"@type":61,"acceptedAnswer":71},"Through which signaling pathway does FEN1 promote progression?",{"text":72,"@type":64},"FEN1 promotes pancreatic cancer progression via regulation of epithelial-mesenchymal transition through the AKT/mTOR signaling pathway.","https://schema.org",{"og:url":32,"og:type":75,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":77,"canonical":32},"index,follow",{"doc_id":79,"site_id":7},374645,1790335908,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,106,110,115,120,123,127],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":85,"show_sort_weight":86,"slug":87},"Story & Novel",90,"story-novel",{"id":26,"doc_module":4,"doc_module_name":25,"category_name":89,"show_sort_weight":90,"slug":91},"Literature",80,"literature",{"id":33,"doc_module":4,"doc_module_name":25,"category_name":93,"show_sort_weight":94,"slug":95},"Exam",70,"exam",{"id":97,"doc_module":4,"doc_module_name":25,"category_name":98,"show_sort_weight":99,"slug":100},5,"Comic",60,"comic",{"id":102,"doc_module":4,"doc_module_name":25,"category_name":103,"show_sort_weight":104,"slug":105},6,"Technology",50,"technology",{"id":107,"doc_module":4,"doc_module_name":25,"category_name":29,"show_sort_weight":108,"slug":109},7,40,"healthcare",{"id":111,"doc_module":4,"doc_module_name":25,"category_name":112,"show_sort_weight":113,"slug":114},8,"Research & Report",30,"research-report",{"id":116,"doc_module":4,"doc_module_name":25,"category_name":117,"show_sort_weight":118,"slug":119},9,"Religion & Spirituality",20,"religion-spirituality",{"id":118,"doc_module":4,"doc_module_name":25,"category_name":121,"show_sort_weight":118,"slug":122},"World Cup","world-cup",{"id":124,"doc_module":4,"doc_module_name":25,"category_name":125,"show_sort_weight":124,"slug":126},10,"Lifestyle","lifestyle",{"id":128,"doc_module":4,"doc_module_name":25,"category_name":129,"show_sort_weight":97,"slug":130},19,"General","general",{"code":4,"msg":82,"data":132},{"doc_id":79,"user_id":133,"nickname":42,"user_avatar":134,"doc_module":4,"category_id":107,"category_name":29,"doc_title":10,"doc_description":12,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":55,"is_deleted":4,"is_public":22,"is_downloadable":22,"audit_status":22,"page_count":128,"language":140,"language_code":8,"site_id":7,"html_lang":8,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":12,"update_tm":144,"read_time":145},2336475401981,"https://ap-avatar.wpscdn.com/avatar/22000c94efd8d5204d?x-image-process=image/resize,m_fixed,w_180,h_180&k=1786935347598174694","| W | J | G | O | World Journal of\u003Cbr>Gastrointestinal Oncology |\n| --- | --- | --- | --- | --- |\n\nSubmit a Manuscript: [https://www.f6publishing.com](https://www.f6publishing.com) World J Gastrointest Oncol 2025 July 15; 17(7): 104402  \nDOI: 10.4251/wjgo.v17.i7.104402 ISSN 1948-5204 (online)  \nORIGINAL ARTICLE  \nBasic Study  \nFlap endonuclease-1 promotes pancreatic cancer progression via AKT/mTOR signaling pathway  \nYu Xia, Na Guo, Cheng-Lou Zhu, Jie-Yun Gao, Ming-Xu Da  \nSpecialty type: Oncology  \nProvenance and peer review:  \nUnsolicited article; Externally peer reviewed.  \nPeer-review model: Single blind  \nPeer-review report’s classification Scientific Quality: Grade A, Grade B, Grade C  \nNovelty: Grade B, Grade B, Grade B  \nCreativity or Innovation: Grade A, Grade B, Grade B  \nScientific Significance: Grade A, Grade B, Grade B  \nP-Reviewer: Wang SJ; Yang F  \nReceived: December 20, 2024  \nRevised: April 8, 2025  \nAccepted: May 29, 2025  \nPublished online: July 15, 2025  \nProcessing time: 207 Days and 5.4 Hours  \nYu Xia, Na Guo, Cheng-Lou Zhu, Ming-Xu Da, The First School of Clinical Medicine, Lanzhou University, Lanzhou 730000, Gansu Province, China  \nJie-Yun Gao, Department of Clinical Teaching, Gansu Provincial Hospital, Lanzhou 730000, Gansu Province, China  \nMing-Xu Da, Department of Surgical Oncology, Gansu Provincial Hospital, Lanzhou 730000, Gansu Province, China  \nCo-first authors: Yu Xia and Na Guo.  \nCo-corresponding authors: Jie-Yun Gao and Ming-Xu Da.  \nCorresponding author: Ming-Xu Da, The First School of Clinical Medicine, Lanzhou University, No. 222 Tianshui South, Chengguan District, Lanzhou 730000, Gansu Province, [China.](China. ldyy_damx@lzu.edu.cn)[ ldyy_damx@lzu.edu.cn](China. ldyy_damx@lzu.edu.cn)  \nAbstract  \nBACKGROUND  \nPancreatic cancer (PC) remains one of the most lethal malignancies. While flap endonuclease-1 (FEN1) has been implicated in various cancers, its role in PC remains unclear.  \nAIM  \nTo investigate the biological functions and mechanisms of FEN1 in PC progression.  \nMETHODS  \nFEN1 expression and its prognostic significance were analyzed using Gene Expression Omnibus, The Cancer Genome Atlas, and Genotype-Tissue Expression databases. FEN1 was knocked down or overexpressed in PC cell lines using lentiviral vectors. Cell proliferation, migration, and invasion were assessed in vitro, while tumorigenicity was evaluated in nude mouse xenografts. Molecular mechanisms were explored through RNA-sequencing and validated by western blot analysis.  \nRESULTS  \nFEN1 was significantly upregulated in PC tissues and correlated with poor prognosis. FEN1 promoted PC cell proliferation, migration, and invasion in vitro,  \n WJGO  [https://www.wjgnet.com](https://www.wjgnet.com) 1 July 15, 2025  Volume 17  Issue 7   \nXia Y et al. The role of FEN1 in PC  \nas well as xenograft tumor growth in vivo. Mechanistically, FEN1 regulated epithelial-mesenchymal transition through the AKT/mTOR signaling pathway.  \nCONCLUSION  \nFEN1 functions as an oncogenic driver in PC progression via the AKT/mTOR signaling pathway, suggesting its potential as a therapeutic target.  \nKey Words: Flap endonuclease-1; Pancreatic cancer; AKT/mTOR signaling pathway; Proliferation; Migration; Invasion  \n©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.  \nCore Tip: This study elucidates the oncogenic role of flap endonuclease-1 (FEN1) in pancreatic cancer (PC), demonstrating its ability to promote cancer cell proliferation, migration, and invasion through modulation of the AKT/mTOR signaling pathway. Elevated FEN1 expression is closely associated with poor prognosis in PC patients, and FEN1 significantly enhances tumor growth both in vitro and in vivo. RNA sequencing, transcriptome analysis, and functional experiments further validate that the oncogenic effects of FEN1 are partially mediated by the activation of the AKT/mTOR signaling pathway, providing compelling evidence for FEN1 as a potential therap","cbCaivlPhCgVyZ2p","https://ap.wps.com/l/cbCaivlPhCgVyZ2p","pdf",53359633,"English","# Abstract\n## Background\n## Aim\n## Methods\n## Results\n## Conclusion\n# Introduction","[{\"question\":\"What is the study purpose regarding FEN1 in pancreatic cancer?\",\"answer\":\"To determine the biological functions and underlying mechanisms of FEN1 during pancreatic cancer progression.\"},{\"question\":\"How was FEN1 function tested in pancreatic cancer models?\",\"answer\":\"FEN1 expression and prognostic significance were analyzed using GEO, TCGA, and GTEx, and FEN1 was knocked down or overexpressed in pancreatic cancer cell lines using lentiviral vectors. Proliferation, migration, and invasion were measured in vitro, while tumor growth was evaluated in nude mouse xenografts.\"},{\"question\":\"Through which signaling pathway does FEN1 promote progression?\",\"answer\":\"FEN1 promotes pancreatic cancer progression via regulation of epithelial-mesenchymal transition through the AKT/mTOR signaling pathway.\"}]","Flap endonuclease-1 promotes pancreatic cancer progression via AKT/mTOR signaling pathway | PDF",1790202086,48]