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GLUT5 过表达相关的肿瘤发生意义。

GLUT5-overexpression-related tumorigenic implications.

机构信息

Institute of Biology, Faculty of Natural Sciences and Mathematics, Ss. Cyril and Methodius University, Skopje, 1000, North Macedonia.

Friedman Diabetes Institute, Lenox Hill Hospital, Northwell Health, 110 E 59th Street, New York, NY, 10022, USA.

出版信息

Mol Med. 2024 Aug 6;30(1):114. doi: 10.1186/s10020-024-00879-8.


DOI:10.1186/s10020-024-00879-8
PMID:39107723
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11304774/
Abstract

Glucose transporter 5 (GLUT5) overexpression has gained increasing attention due to its profound implications for tumorigenesis. This manuscript provides a comprehensive overview of the key findings and implications associated with GLUT5 overexpression in cancer. GLUT5 has been found to be upregulated in various cancer types, leading to alterations in fructose metabolism and enhanced glycolysis, even in the presence of oxygen, a hallmark of cancer cells. This metabolic shift provides cancer cells with an alternative energy source and contributes to their uncontrolled growth and survival. Beyond its metabolic roles, recent research has unveiled additional aspects of GLUT5 in cancer biology. GLUT5 overexpression appears to play a critical role in immune evasion mechanisms, which further worsens tumor progression and complicates therapeutic interventions. This dual role of GLUT5 in both metabolic reprogramming and immune modulation highlights its significance as a potential diagnostic marker and therapeutic target. Understanding the molecular mechanisms driving GLUT5 overexpression is crucial for developing targeted therapeutic strategies that can disrupt the unique vulnerabilities of GLUT5-overexpressing cancer cells. This review emphasizes the complexities surrounding GLUT5's involvement in cancer and underscores the pressing need for continued research to unlock its potential as a diagnostic biomarker and therapeutic target, ultimately improving cancer management and patient outcomes.

摘要

葡萄糖转运蛋白 5(GLUT5)的过表达因其对肿瘤发生的深远影响而受到越来越多的关注。本文综述了 GLUT5 过表达在癌症中的关键发现和意义。已经发现 GLUT5 在各种癌症类型中上调,导致果糖代谢改变和糖酵解增强,即使在氧气存在的情况下,这也是癌细胞的一个标志。这种代谢转变为癌细胞提供了一种替代能源,并促进其不受控制的生长和存活。除了其代谢作用外,最近的研究还揭示了 GLUT5 在癌症生物学中的其他方面。GLUT5 过表达似乎在免疫逃逸机制中发挥关键作用,这进一步恶化了肿瘤的进展,并使治疗干预复杂化。GLUT5 在代谢重编程和免疫调节中的双重作用突出了其作为潜在诊断标志物和治疗靶点的重要性。了解驱动 GLUT5 过表达的分子机制对于开发靶向治疗策略至关重要,这些策略可以破坏 GLUT5 过表达癌细胞的独特脆弱性。本综述强调了 GLUT5 参与癌症的复杂性,并强调了继续研究以释放其作为诊断生物标志物和治疗靶点的潜力的迫切需要,最终改善癌症管理和患者预后。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dc9/11304774/2f4aebe64d36/10020_2024_879_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dc9/11304774/ab9ffaeecd5a/10020_2024_879_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dc9/11304774/cee4fdf3f554/10020_2024_879_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dc9/11304774/2ee66044d635/10020_2024_879_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dc9/11304774/2f4aebe64d36/10020_2024_879_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dc9/11304774/ab9ffaeecd5a/10020_2024_879_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dc9/11304774/cee4fdf3f554/10020_2024_879_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dc9/11304774/2ee66044d635/10020_2024_879_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dc9/11304774/2f4aebe64d36/10020_2024_879_Fig4_HTML.jpg

相似文献

[1]
GLUT5-overexpression-related tumorigenic implications.

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[2]
Dietary Fructose Promotes Prostate Cancer Growth.

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[3]
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[4]
GLUT5: structure, functions, diseases and potential applications.

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[5]
Regulation of the fructose transporter GLUT5 in health and disease.

Am J Physiol Endocrinol Metab. 2008-8

[6]
Diet-induced epigenetic regulation in vivo of the intestinal fructose transporter Glut5 during development of rat small intestine.

Biochem J. 2011-4-1

[7]
GLUT5-KHK axis-mediated fructose metabolism drives proliferation and chemotherapy resistance of colorectal cancer.

Cancer Lett. 2022-5-28

[8]
GLUT5-mediated fructose utilization drives lung cancer growth by stimulating fatty acid synthesis and AMPK/mTORC1 signaling.

JCI Insight. 2020-2-13

[9]
Developmental reprogramming of rat GLUT5 requires glucocorticoid receptor translocation to the nucleus.

J Physiol. 2008-8-1

[10]
Fructose utilization enhanced by GLUT5 promotes lung cancer cell migration via activating glycolysis/AKT pathway.

Clin Transl Oncol. 2023-4

引用本文的文献

[1]
Fructose metabolism and its roles in metabolic diseases, inflammatory diseases, and cancer.

Mol Biomed. 2025-6-23

[2]
Fructose Metabolism in Cancer: Molecular Mechanisms and Therapeutic Implications.

Int J Med Sci. 2025-6-9

[3]
Role of fructose in renal cell carcinoma progression.

Discov Oncol. 2025-5-23

本文引用的文献

[1]
It's a Trap! Aldolase-Prescribed C Deoxyradiofluorination Affords Intracellular Trapping and the Tracing of Fructose Metabolism by PET.

J Nucl Med. 2024-3-1

[2]
Biological role of fructose in the male reproductive system: Potential implications for prostate cancer.

Prostate. 2024-1

[3]
Molecular profiling reveals potential targets in cholangiocarcinoma.

World J Gastroenterol. 2023-7-7

[4]
Hexokinases in cancer and other pathologies.

Cell Insight. 2023-1-3

[5]
A Fluorescence-Based Assay to Probe Inhibitory Effect of Fructose Mimics on GLUT5 Transport in Breast Cancer Cells.

ACS Bio Med Chem Au. 2022-11-7

[6]
Trichostatin A inhibits expression of the human SLC2A5 gene via SNAI1/SNAI2 transcription factors and sensitizes colon cancer cells to platinum compounds.

Eur J Pharmacol. 2023-6-15

[7]
GLUT-Targeting Phototherapeutic Nanoparticles for Synergistic Triple Combination Cancer Therapy.

ACS Appl Mater Interfaces. 2023-2-13

[8]
Late-Stage Functionalization through Click Chemistry Provides GLUT5-Targeting Glycoconjugate as a Potential PET Imaging Probe.

Int J Mol Sci. 2022-12-22

[9]
Targeting fructose metabolism by glucose transporter 5 regulation in human cholangiocarcinoma.

Genes Dis. 2021-10-2

[10]
Transcriptional regulation of glucose transporters in human oral squamous cell carcinoma cells.

J Oral Pathol Med. 2022-9

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