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胰腺癌中葡萄糖代谢的重编程:机制、影响及治疗前景

Reprogramming of glucose metabolism in pancreatic cancer: mechanisms, implications, and therapeutic perspectives.

作者信息

Zhang Yan, Li Wancheng, Niu Jubao, Fan Zeyang, Li Xin, Zhang Hui

机构信息

The Second Clinical Medical School, Lanzhou University, Lanzhou, China.

Department of General Surgery, The Second Hospital of Lanzhou University, The Second Clinical Medical School, Lanzhou University, Lanzhou, China.

出版信息

Front Immunol. 2025 Jun 24;16:1586959. doi: 10.3389/fimmu.2025.1586959. eCollection 2025.

DOI:10.3389/fimmu.2025.1586959
PMID:40630951
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12234474/
Abstract

As a typical pathological feature of pancreatic ductal adenocarcinoma, reprogramming of glucose metabolism synergistically drives the tumorigenesis and development process through molecular mechanisms such as regulating the expression of driver genes, modifying key functional proteins, triggering mitochondrial metabolism abnormality, and remodeling the tumor microenvironment. It is worth noting that this metabolic remodeling phenomenon is significantly associated with the formation of chemoresistance. Based on the latest research progress, this paper systematically describes the molecular basis of glucose metabolic reprogramming in pancreatic cancer, drug resistance characteristics and its targeted intervention strategies, and provides a theoretical framework for the research and development of innovative drugs.

摘要

作为胰腺导管腺癌的典型病理特征,葡萄糖代谢重编程通过调节驱动基因表达、修饰关键功能蛋白、引发线粒体代谢异常以及重塑肿瘤微环境等分子机制,协同驱动肿瘤发生和发展过程。值得注意的是,这种代谢重塑现象与化疗耐药的形成显著相关。基于最新研究进展,本文系统阐述了胰腺癌中葡萄糖代谢重编程的分子基础、耐药特征及其靶向干预策略,为创新药物研发提供理论框架。

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本文引用的文献

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Pancreatic cancer subtyping - the keystone of precision treatment.胰腺癌亚型分类——精准治疗的关键
Front Immunol. 2025 Apr 8;16:1563725. doi: 10.3389/fimmu.2025.1563725. eCollection 2025.
2
Targeting KRAS: from metabolic regulation to cancer treatment.靶向KRAS:从代谢调控到癌症治疗
Mol Cancer. 2025 Jan 11;24(1):9. doi: 10.1186/s12943-024-02216-3.
3
ITGA3 promotes pancreatic cancer progression through HIF1α- and c-Myc-driven glycolysis in a collagen I-dependent autocrine manner.整合素α3(ITGA3)通过低氧诱导因子1α(HIF1α)和c-Myc驱动的糖酵解,以I型胶原蛋白依赖性自分泌方式促进胰腺癌进展。
Cancer Gene Ther. 2025 Feb;32(2):240-253. doi: 10.1038/s41417-024-00864-7. Epub 2024 Dec 17.
4
Neutrophils in cancer: from biology to therapy.癌症中的中性粒细胞:从生物学至治疗
Cell Mol Immunol. 2025 Jan;22(1):4-23. doi: 10.1038/s41423-024-01244-9. Epub 2024 Dec 9.
5
GLUT1 overexpression in CAR-T cells induces metabolic reprogramming and enhances potency.CAR-T 细胞中 GLUT1 的过表达诱导代谢重编程并增强效力。
Nat Commun. 2024 Oct 6;15(1):8658. doi: 10.1038/s41467-024-52666-y.
6
Dynamic glycolytic reprogramming effects on dendritic cells in pancreatic ductal adenocarcinoma.动态糖酵解重编程对胰腺导管腺癌树突状细胞的影响。
J Exp Clin Cancer Res. 2024 Sep 30;43(1):271. doi: 10.1186/s13046-024-03192-8.
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AARS1 and AARS2 sense L-lactate to regulate cGAS as global lysine lactyltransferases.AARS1 和 AARS2 通过感知 L-乳酸来作为全局赖氨酸酰基转移酶调节 cGAS。
Nature. 2024 Oct;634(8036):1229-1237. doi: 10.1038/s41586-024-07992-y. Epub 2024 Sep 25.
8
Metabolic landscape of the healthy pancreas and pancreatic tumor microenvironment.健康胰腺和胰腺肿瘤微环境的代谢全景。
JCI Insight. 2024 Aug 13;9(18):e180114. doi: 10.1172/jci.insight.180114.
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Commun Biol. 2024 Aug 30;7(1):1065. doi: 10.1038/s42003-024-06760-y.
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Clin Transl Med. 2024 Aug;14(8):e70003. doi: 10.1002/ctm2.70003.