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胃癌代谢重编程的研究进展

Advances in the Study of Metabolic Reprogramming in Gastric Cancer.

作者信息

Rong Yu, Teng Yuanyin, Zhou Xiaoying

机构信息

The First Clinical Medical College, Nanjing Medical University, Nanjing, China.

The Second Clinical Medical College, Nanjing Medical University, Nanjing, China.

出版信息

Cancer Med. 2025 May;14(10):e70948. doi: 10.1002/cam4.70948.

DOI:10.1002/cam4.70948
PMID:40365984
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12076355/
Abstract

BACKGROUND

Gastric cancer is one of the most prevalent malignancies of the digestive system and is associated with a poor prognosis, particularly in advanced metastatic stages, where the 5-year survival rate is significantly low.

METHODS

Recent research has demonstrated that metabolic reprogramming-including alterations in glucose, lipid, and amino-acid metabolism-plays a critical role in both the development and progression of this disease. To gain deeper insights into these metabolic shifts, scientists have increasingly employed metabolomics, a non-invasive technique that detects and quantifies small molecules within cancerous tissues, thereby enhancing prognostic assessments.

AIM

Analyzing the metabolic profiles of gastric-cancer tissues can reveal significant changes in key metabolic pathways, which may open new avenues for targeted therapies and ultimately improve patient outcomes.

CONCLUSION

This article reviews recent advancements in the study of metabolic reprogramming in gastric cancer, aiming to identify potential therapeutic targets and offer new hope to patients.

摘要

背景

胃癌是消化系统最常见的恶性肿瘤之一,预后较差,尤其是在晚期转移阶段,5年生存率极低。

方法

最近的研究表明,代谢重编程——包括葡萄糖、脂质和氨基酸代谢的改变——在这种疾病的发生和发展中都起着关键作用。为了更深入地了解这些代谢变化,科学家们越来越多地采用代谢组学,这是一种非侵入性技术,可检测和量化癌组织内的小分子,从而加强预后评估。

目的

分析胃癌组织的代谢谱可揭示关键代谢途径的显著变化,这可能为靶向治疗开辟新途径,并最终改善患者预后。

结论

本文综述了胃癌代谢重编程研究的最新进展,旨在确定潜在的治疗靶点并为患者带来新希望。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a63a/12076355/ed5c278a6f3b/CAM4-14-e70948-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a63a/12076355/e1d6429e8401/CAM4-14-e70948-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a63a/12076355/ed5c278a6f3b/CAM4-14-e70948-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a63a/12076355/e1d6429e8401/CAM4-14-e70948-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a63a/12076355/ed5c278a6f3b/CAM4-14-e70948-g001.jpg

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本文引用的文献

1
Metabolomic machine learning predictor for diagnosis and prognosis of gastric cancer.代谢组学机器学习预测因子用于胃癌的诊断和预后。
Nat Commun. 2024 Feb 23;15(1):1657. doi: 10.1038/s41467-024-46043-y.
2
Targeting one-carbon metabolism for cancer immunotherapy.靶向一碳代谢用于癌症免疫治疗。
Clin Transl Med. 2024 Jan;14(1):e1521. doi: 10.1002/ctm2.1521.
3
Oncogenic Fatty Acid Metabolism Rewires Energy Supply Chain in Gastric Carcinogenesis.致癌性脂肪酸代谢重塑胃癌发生过程中的能量供应链。
Gastroenterology. 2024 May;166(5):772-786.e14. doi: 10.1053/j.gastro.2024.01.027. Epub 2024 Jan 24.
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Glucose transporter 3 (GLUT3) promotes lactylation modifications by regulating lactate dehydrogenase A (LDHA) in gastric cancer.葡萄糖转运蛋白3(GLUT3)通过调节胃癌中的乳酸脱氢酶A(LDHA)促进乳酸化修饰。
Cancer Cell Int. 2023 Dec 1;23(1):303. doi: 10.1186/s12935-023-03162-8.
5
The microprotein encoded by exosomal lncAKR1C2 promotes gastric cancer lymph node metastasis by regulating fatty acid metabolism.外泌体 lncAKR1C2 编码的微蛋白通过调节脂肪酸代谢促进胃癌淋巴结转移。
Cell Death Dis. 2023 Oct 30;14(10):708. doi: 10.1038/s41419-023-06220-1.
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Lipid metabolic reprogramming in tumor microenvironment: from mechanisms to therapeutics.肿瘤微环境中的脂质代谢重编程:从机制到治疗。
J Hematol Oncol. 2023 Sep 12;16(1):103. doi: 10.1186/s13045-023-01498-2.
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The pentose phosphate pathway in health and disease.戊糖磷酸途径与健康和疾病。
Nat Metab. 2023 Aug;5(8):1275-1289. doi: 10.1038/s42255-023-00863-2. Epub 2023 Aug 23.
8
m5C-methylated lncRNA NR_033928 promotes gastric cancer proliferation by stabilizing GLS mRNA to promote glutamine metabolism reprogramming.m5C 甲基化长非编码 RNA NR_033928 通过稳定 GLS mRNA 促进谷氨酰胺代谢重编程来促进胃癌增殖。
Cell Death Dis. 2023 Aug 15;14(8):520. doi: 10.1038/s41419-023-06049-8.
9
Loss of RACK1 promotes glutamine addiction via activating AKT/mTOR/ASCT2 axis to facilitate tumor growth in gastric cancer.RACK1 缺失通过激活 AKT/mTOR/ASCT2 轴促进谷氨酰胺成瘾,从而促进胃癌的肿瘤生长。
Cell Oncol (Dordr). 2024 Feb;47(1):113-128. doi: 10.1007/s13402-023-00854-1. Epub 2023 Aug 14.
10
Targeting TLK2 inhibits the progression of gastric cancer by reprogramming amino acid metabolism through the mTOR/ASNS axis.靶向 TLK2 通过 mTOR/ASNS 轴重编程氨基酸代谢抑制胃癌的进展。
Cancer Gene Ther. 2023 Nov;30(11):1485-1497. doi: 10.1038/s41417-023-00653-8. Epub 2023 Aug 4.