Chengqiang Wang, Lu Wang, Qing Zhao, Jiao Ma, Yitao Li, Junliang Kuang, Xintong Yang, Huichang Bi, Aiping Lu, Kenneth C. P. Cheung, Gerry Melino, Wei Jia
{"title":"Exploring fructose metabolism as a potential therapeutic approach for pancreatic cancer","authors":"Chengqiang Wang, Lu Wang, Qing Zhao, Jiao Ma, Yitao Li, Junliang Kuang, Xintong Yang, Huichang Bi, Aiping Lu, Kenneth C. P. Cheung, Gerry Melino, Wei Jia","doi":"10.1038/s41418-024-01394-3","DOIUrl":null,"url":null,"abstract":"<p>Excessive fructose intake has been associated with the development and progression of pancreatic cancer. This study aimed to elucidate the relationship between fructose utilization and pancreatic cancer progression. Our findings revealed that pancreatic cancer cells have a high capacity to utilize fructose and are capable of converting glucose to fructose via the <i>AKR1B1</i>-mediated polyol pathway, in addition to uptake via the fructose transporter GLUT5. Fructose metabolism exacerbates pancreatic cancer proliferation by enhancing glycolysis and accelerating the production of key metabolites that regulate angiogenesis. However, pharmacological blockade of fructose metabolism has been shown to slow pancreatic cancer progression and synergistically enhance anti-tumor capabilities when combined with anti-angiogenic agents. Overall, targeting fructose metabolism may prove to be a promising therapeutic approach in the treatment of pancreatic cancer.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"81 1","pages":""},"PeriodicalIF":13.7000,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Death and Differentiation","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1038/s41418-024-01394-3","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Excessive fructose intake has been associated with the development and progression of pancreatic cancer. This study aimed to elucidate the relationship between fructose utilization and pancreatic cancer progression. Our findings revealed that pancreatic cancer cells have a high capacity to utilize fructose and are capable of converting glucose to fructose via the AKR1B1-mediated polyol pathway, in addition to uptake via the fructose transporter GLUT5. Fructose metabolism exacerbates pancreatic cancer proliferation by enhancing glycolysis and accelerating the production of key metabolites that regulate angiogenesis. However, pharmacological blockade of fructose metabolism has been shown to slow pancreatic cancer progression and synergistically enhance anti-tumor capabilities when combined with anti-angiogenic agents. Overall, targeting fructose metabolism may prove to be a promising therapeutic approach in the treatment of pancreatic cancer.
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