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Bioinformatics and clinical sample analyses, combined with xenograft models, metabolic screening, and RNA sequencing, were used to define mechanisms. F. nucleatum accumulates at OSCC invasive margins and promotes tumor-associated macrophage formation through GalNAc-mediated autophagy-TBC1D5 signaling, driving GLUT1 aggregation and extracellular lactate deposition. Inhibiting GalNAc and GLUT1 reduces TAMs and restrains OSCC progression.",{"@graph":69,"@context":123},[70,84,106],{"@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":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/f-nucleatum-facilitates-oral-squamous-cell-carcinoma-progression-via-glut1-driven-lactate-production/377559/",{"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/f-nucleatum-facilitates-oral-squamous-cell-carcinoma-progression-via-glut1-driven-lactate-production/377559.png","ImageObject",300,407,{"name":92,"@type":93},"LangkahRina","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-30","2026-09-24",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",15,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"What role does F. nucleatum play in OSCC progression?","Question",{"text":113,"@type":114},"F. nucleatum accumulates in invasive margins of OSCC tissues and drives tumor-associated macrophage (TAM) formation, promoting OSCC progression.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"How does F. nucleatum regulate lactate production and GLUT1?",{"text":118,"@type":114},"OSCC-resident F. nucleatum triggers GalNAc-autophagy-TBC1D5 signaling, leading to GLUT1 aggregation in the plasma membrane and extracellular lactate deposition.",{"name":120,"@type":111,"acceptedAnswer":121},"What therapeutic strategy does the study suggest?",{"text":122,"@type":114},"Simultaneous functional inhibition of GalNAc and GLUT1 efficiently reduces TAM formation and restrains OSCC progression, indicating a targeted clinical intervention potential.","https://schema.org",{"og:url":83,"og:type":125,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":127,"canonical":83},"index,follow",{"doc_id":129,"site_id":62},377559,1790632258,{"code":4,"msg":5,"data":132},{"doc_id":129,"user_id":133,"nickname":92,"user_avatar":134,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":105,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":46,"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":31},962090893776,"https://ap-avatar.wpscdn.com/davatar_155a257f0dc6eb9ab79c44ca47cae57d","Articles   \nF. nucleatum facilitates oral squamous cell carcinoma progression via GLUT1-driven lactate production  \nJiwei Sun,a,b,c,f Qingming Tang,a,b,c,f Shaoling Yu,a,b,c Mengru Xie,a,b,c Wenhao Zheng,a,b,c Guangjin Chen,a,b,c Ying Yin,a,b,c Xiaofei Huang,a,b,c Keqi Wo,a,b,c Haoqi Lei,a,b,c Junyuan Zhang,a,b,c Qian Wan,d,e and Lili Chena,b,c,∗  \naDepartment of Stomatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China  \nbSchool of Stomatology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China cHubei Province Key Laboratory of Oral and Maxillofacial Development and Regeneration, Wuhan, 430022, China  \ndHubei Key Laboratory of Natural Medicinal Chemistry and Resource Evaluation, School of Pharmacy, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan, 430030, Hubei, China  \neInstitute of Brain Research, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan, 430030, Hubei, China  \nSummary  \nBackground Tumor-resident microbiota has been documented for various cancer types. Oral squamous cell carcinoma (OSCC) is also enriched with microbiota, while the significance of microbiota in shaping the OSCC microenvironment remains elusive.  \nMethods We used bioinformatics and clinical sample analysis to explore relationship between F. nucleatum and OSCC progression. Xenograft tumor model, metabolic screening and RNA sequencing were performed to elucidate mechanisms of pro-tumor role of F. nucleatum.  \nFindings We show that a major protumorigenic bacterium, F. nucleatum, accumulates in invasive margins ofOSCC tissues and drives tumor-associated macrophages (TAMs) formation. The mechanistic dissection shows that OSCCresident F. nucleatum triggers the GalNAc-Autophagy-TBC1D5 signaling, leading to GLUT1 aggregation in the plasma membrane and the deposition of extracellular lactate. Simultaneous functional inhibition of GalNAc and GLUT1 efficiently reduces TAMs formation and restrains OSCC progression.  \nInterpretation These findings suggest that tumor-resident microbiota affects the immunomodulatory and protumorigenic microenvironment via modulating glycolysis and extracellular lactate deposition. The targeted intervention of this process could provide a distinct clinical strategy for patients with advanced OSCC.  \nFunding This work was supported by the National Natural Science Foundation of China for Key Program Projects (82030070, to LC) and Distinguished Young Scholars (31725011, to LC), as well as Innovation Team Project of Hubei Province (2020CFA014, to LC) .  \nCopyright © 2023 The Author(s) . Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license ([http://creativecommons.org/licenses/by-nc-nd/4.0/](http://creativecommons.org/licenses/by-nc-nd/4.0/)).  \nKeywords: Oral squamous cell carcinoma; F. nucleatum; Tumor-associated macrophage; GLUT1; Autophagy  \nIntroduction  \nOral squamous cell carcinoma (OSCC) is a prevalent subtype of head and neck squamous cell carcinoma (HNSCC) .1–3 Despite progress in the diagnosis and treatment of OSCC, the 5-year survival rate remains low due to metastasis or recurrence.4 , 5 Cohort studies have suggested that, in addition to the genetic, epigenetic, and stromal microenvironment elements, the features of the microbiota within tissues are associated with the hallmarks of cancer, including risks,  \npathological types, and prognosis.6–10 Likewise, given that OSCC originates in the microbiota-enriched oral cavity, the microbiota emerges as a non-negligible potential mediator regulating OSCC progression.11–14 F. nucleatum is a gram-negative anaerobic bacterium and has been suggested as a major protumorigenic bacterium compared with other oral bacteria.15 , 16 However, as the constituent species of OSCC microbiota, how F. nucleatum affects the progression of OSCC remains largely unexplored.  \n*Corresponding author. Department of Stomatology, U","cbCaiihdq4KdQJgl","https://ap.wps.com/l/cbCaiihdq4KdQJgl","pdf",6826948,"English","# Summary\n# Introduction\n# Research in context\n## Evidence before this study\n## Added value of this study\n## Implications of all the available evidence","[{\"question\":\"What role does F. nucleatum play in OSCC progression?\",\"answer\":\"F. nucleatum accumulates in invasive margins of OSCC tissues and drives tumor-associated macrophage (TAM) formation, promoting OSCC progression.\"},{\"question\":\"How does F. nucleatum regulate lactate production and GLUT1?\",\"answer\":\"OSCC-resident F. nucleatum triggers GalNAc-autophagy-TBC1D5 signaling, leading to GLUT1 aggregation in the plasma membrane and extracellular lactate deposition.\"},{\"question\":\"What therapeutic strategy does the study suggest?\",\"answer\":\"Simultaneous functional inhibition of GalNAc and GLUT1 efficiently reduces TAM formation and restrains OSCC progression, indicating a targeted clinical intervention potential.\"}]","F. nucleatum facilitates oral squamous cell carcinoma progression via GLUT1-driven lactate production | PDF",1790225958]