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Although glucose is traditionally viewed as the main carbon source, fructose is described as an alternative substrate that drives tumor growth, metastasis, and treatment resistance. The review details how fructose metabolism, through KHK, ALDOB, and GLUT5, promotes glycolysis, lipid synthesis, and nucleotide production, particularly under glucose-limited conditions, and outlines therapeutic targeting implications.",{"@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/fructose-metabolism-in-cancer-molecular-mechanismsand-therapeutic-implications-review/369582/",{"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/fructose-metabolism-in-cancer-molecular-mechanismsand-therapeutic-implications-review/369582.png","ImageObject",300,407,{"name":92,"@type":93},"วิน","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-30","2026-09-23",true,{"@type":102,"interactionType":103,"userInteractionCount":105},"InteractionCounter",{"@type":104},"ViewAction",12,{"@type":107,"mainEntity":108},"FAQPage",[109,115,119],{"name":110,"@type":111,"acceptedAnswer":112},"Why is fructose metabolism relevant to cancer cells?","Question",{"text":113,"@type":114},"Fructose metabolism provides an alternative carbon source that supports tumor growth, metastasis, and resistance to therapy, especially under metabolic stress.","Answer",{"name":116,"@type":111,"acceptedAnswer":117},"Which key components regulate fructose metabolism in cancer?",{"text":118,"@type":114},"The review highlights ketohexokinase (KHK), aldolase B (ALDOB), and the fructose transporter GLUT5 as crucial elements supporting fructose-driven metabolic programs.",{"name":120,"@type":111,"acceptedAnswer":121},"How does hypoxia influence fructose production in the tumor microenvironment?",{"text":122,"@type":114},"Oxygen deprivation, rather than glucose scarcity, is presented as the main trigger, with HIF-1α upregulating AR and SDH to drive glucose conversion toward fructose via the polyol pathway.","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},369582,1790511956,{"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":140,"language":141,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":142,"faqs":143,"seo_title":144,"seo_description":67,"update_tm":145,"read_time":146},2336475104736,"https://ap-avatar.wpscdn.com/avatar/22000c4c5e0e5b17e70?x-image-process=image/resize,m_fixed,w_180,h_180&k=1786591360781797222","Ivyspring  \nInternational Publisher  \nInternationalJournal of Medical Sciences  \n2025; 22(11): 2852-2876. doi: 10.7150/ijms.108549  \nReview  \nFructose Metabolism in Cancer: Molecular Mechanismsand Therapeutic Implications  \nXinyi Chen, Mu Yang, Lu Wang, Jingyao Tu􀀍, Xianglin Yuan􀀍  \nDepartment of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.  \n􀀍 Corresponding authors: Xianglin Yuan, Department of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China. Address: Jie Fang Road 1095, Wuhan, China; Tel.: +8602783662683; Fax: +8602783662683; E-mail address: [yuanxianglin@hust.edu.cn. Jingyao Tu](yuanxianglin@hust.edu.cn. Jingyao Tu), Department of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China; Address: Jie Fang Road 1095, Wuhan, China; E-mail address: [tujingyao0702@163.com](tujingyao0702@163.com).  \n© The author(s). This is an open access article distributed under the terms of the Creative Commons Attribution License ([https://creativecommons.org/licenses/by/4.0/](https://creativecommons.org/licenses/by/4.0/)). See [https://ivyspring.com/terms](https://ivyspring.com/terms) for full terms and conditions.  \nReceived: 2024.12.10; Accepted: 2025.05.16; Published: 2025.06.09  \nAbstract  \nMetabolic reprogramming enables cancer cells to adapt to the tumor microenvironment, facilitating their survival, proliferation, and resistance to therapy. While glucose has long been considered the primary substrate for cancer cell metabolism, recent studies have highlighted the role of fructose as an alternative carbon source. Fructose metabolism, particularly through key enzymes such as ketohexokinase (KHK) and aldolase B (ALDOB), along with the fructose transporter GLUT5, supports tumor growth, metastasis, and therapeutic resistance. This review explores the mechanisms by which fructose metabolism influences cancer progression, focusing on its metabolic pathways and its impact on the tumor microenvironment. By promoting glycolysis, lipid biosynthesis, and nucleotide production, fructose metabolism enhances the metabolic adaptability of cancer cells, especially in glucose-deprived conditions. A comprehensive understanding of these processes offers potential insights into therapeutic strategies targeting fructose metabolism for cancer treatment. However, further studies are required to fully elucidate the complex role of fructose in various malignancies.  \nKeywords: fructose metabolism; tumor metabolism; metabolic reprogramming; ketohexokinase; aldolase; glucose transporter  \n1. Introduction  \nThrough metabolic reprogramming, cancer cells can progressively acquire necessary adaptations for survival within the tumor microenvironment (TME) . These adaptations are vital for supporting elevated synthetic demands and aggressive proliferation, consequently enhancing resistance to anti-tumor immunity. Otto Warburg's investigations into cancer cell metabolism in the 1920s identified an unexpected phenomenon: cancer cells were found to convert glucose to lactate more effectively than normal tissues, even in well-oxygenated environments. Warburg theorized that this increased glycolysis was due to underlying mitochondrial dysfunction, a concept now known as the Warburg effect (1, 2) . Glycolysis, although less efficient in ATP generation than mitochondrial oxidative respiration, is essential for generating intermediates utilized for synthesizing amino acids, lipids, and nucleotides. These  \nintermediates, therefore, support the increased demands of tumor cells for proliferation and enduring therapeutic resistance (3) . Investigating the interplay between cancer glycolysis and the metabolic dysregulation characteristic of metabolic syndrome could potentially identify novel therapeutic targetsand deepen the understanding of their interrelatio","cbCaikkHAqSLTqiy","https://ap.wps.com/l/cbCaikkHAqSLTqiy","pdf",2135405,25,"English","# Introduction\n# Abstract\n# Keywords\n# Fructose Metabolism in Cancer - Molecular Mechanismsand Therapeutic Implications - Review","[{\"question\":\"Why is fructose metabolism relevant to cancer cells?\",\"answer\":\"Fructose metabolism provides an alternative carbon source that supports tumor growth, metastasis, and resistance to therapy, especially under metabolic stress.\"},{\"question\":\"Which key components regulate fructose metabolism in cancer?\",\"answer\":\"The review highlights ketohexokinase (KHK), aldolase B (ALDOB), and the fructose transporter GLUT5 as crucial elements supporting fructose-driven metabolic programs.\"},{\"question\":\"How does hypoxia influence fructose production in the tumor microenvironment?\",\"answer\":\"Oxygen deprivation, rather than glucose scarcity, is presented as the main trigger, with HIF-1α upregulating AR and SDH to drive glucose conversion toward fructose via the polyol pathway.\"}]","Fructose Metabolism in Cancer - Molecular Mechanismsand Therapeutic Implications - Review | PDF",1790183542,63]