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- Publisher Website: 10.1038/s41418-024-01394-3
- Scopus: eid_2-s2.0-85206844065
- PMID: 39406919
- WOS: WOS:001332771400002
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Article: Exploring fructose metabolism as a potential therapeutic approach for pancreatic cancer
| Title | Exploring fructose metabolism as a potential therapeutic approach for pancreatic cancer |
|---|---|
| Authors | |
| Issue Date | 1-Dec-2024 |
| Publisher | Springer Nature |
| Citation | Cell Death & Differentiation, 2024, v. 31, n. 12, p. 1625-1635 How to Cite? |
| 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. |
| Persistent Identifier | http://hdl.handle.net/10722/358211 |
| ISSN | 2023 Impact Factor: 13.7 2023 SCImago Journal Rankings: 4.102 |
| ISI Accession Number ID |
| DC Field | Value | Language |
|---|---|---|
| dc.contributor.author | Wang, Chengqiang | - |
| dc.contributor.author | Wang, Lu | - |
| dc.contributor.author | Zhao, Qing | - |
| dc.contributor.author | Ma, Jiao | - |
| dc.contributor.author | Li, Yitao | - |
| dc.contributor.author | Kuang, Junliang | - |
| dc.contributor.author | Yang, Xintong | - |
| dc.contributor.author | Bi, Huichang | - |
| dc.contributor.author | Lu, Aiping | - |
| dc.contributor.author | Cheung, Kenneth CP | - |
| dc.contributor.author | Melino, Gerry | - |
| dc.contributor.author | Jia, Wei | - |
| dc.date.accessioned | 2025-07-26T00:30:23Z | - |
| dc.date.available | 2025-07-26T00:30:23Z | - |
| dc.date.issued | 2024-12-01 | - |
| dc.identifier.citation | Cell Death & Differentiation, 2024, v. 31, n. 12, p. 1625-1635 | - |
| dc.identifier.issn | 1350-9047 | - |
| dc.identifier.uri | http://hdl.handle.net/10722/358211 | - |
| dc.description.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 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.</p> | - |
| dc.language | eng | - |
| dc.publisher | Springer Nature | - |
| dc.relation.ispartof | Cell Death & Differentiation | - |
| dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
| dc.title | Exploring fructose metabolism as a potential therapeutic approach for pancreatic cancer | - |
| dc.type | Article | - |
| dc.identifier.doi | 10.1038/s41418-024-01394-3 | - |
| dc.identifier.pmid | 39406919 | - |
| dc.identifier.scopus | eid_2-s2.0-85206844065 | - |
| dc.identifier.volume | 31 | - |
| dc.identifier.issue | 12 | - |
| dc.identifier.spage | 1625 | - |
| dc.identifier.epage | 1635 | - |
| dc.identifier.eissn | 1476-5403 | - |
| dc.identifier.isi | WOS:001332771400002 | - |
| dc.identifier.issnl | 1350-9047 | - |
