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肝癌代谢重编程与肿瘤微环境之间的相互作用。

Interactions between the metabolic reprogramming of liver cancer and tumor microenvironment.

作者信息

Yang Haoqiang, Li Jinghui, Niu Yiting, Zhou Tao, Zhang Pengyu, Liu Yang, Li Yanjun

机构信息

Third Hospital of Shanxi Medical University, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Taiyuan, China.

Department of Hepatobiliary Surgery, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, TongjiShanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, Shanxi, China.

出版信息

Front Immunol. 2025 Feb 14;16:1494788. doi: 10.3389/fimmu.2025.1494788. eCollection 2025.

DOI:10.3389/fimmu.2025.1494788
PMID:40028341
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11868052/
Abstract

Metabolic reprogramming is one of the major biological features of malignant tumors, playing a crucial role in the initiation and progression of cancer. The tumor microenvironment consists of various non-cancer cells, such as hepatic stellate cells, cancer-associated fibroblasts (CAFs), immune cells, as well as extracellular matrix and soluble substances. In liver cancer, metabolic reprogramming not only affects its own growth and survival but also interacts with other non-cancer cells by influencing the expression and release of metabolites and cytokines (such as lactate, PGE2, arginine). This interaction leads to acidification of the microenvironment and restricts the uptake of nutrients by other non-cancer cells, resulting in metabolic competition and symbiosis. At the same time, metabolic reprogramming in neighboring cells during proliferation and differentiation processes also impacts tumor immunity. This article provides a comprehensive overview of the metabolic crosstalk between liver cancer cells and their tumor microenvironment, deepening our understanding of relevant findings and pathways. This contributes to further understanding the regulation of cancer development and immune evasion mechanisms while providing assistance in advancing personalized therapies targeting metabolic pathways for anti-cancer treatment.

摘要

代谢重编程是恶性肿瘤的主要生物学特征之一,在癌症的发生和发展中起着关键作用。肿瘤微环境由各种非癌细胞组成,如肝星状细胞、癌症相关成纤维细胞(CAF)、免疫细胞以及细胞外基质和可溶性物质。在肝癌中,代谢重编程不仅影响其自身的生长和存活,还通过影响代谢产物和细胞因子(如乳酸、PGE2、精氨酸)的表达和释放与其他非癌细胞相互作用。这种相互作用导致微环境酸化,并限制其他非癌细胞对营养物质的摄取,从而导致代谢竞争和共生。同时,邻近细胞在增殖和分化过程中的代谢重编程也会影响肿瘤免疫。本文全面概述了肝癌细胞与其肿瘤微环境之间的代谢串扰,加深了我们对相关发现和途径的理解。这有助于进一步理解癌症发展的调控和免疫逃逸机制,同时为推进针对代谢途径的个性化抗癌治疗提供帮助。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b6/11868052/877d9a44e46e/fimmu-16-1494788-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b6/11868052/13517668f1fb/fimmu-16-1494788-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b6/11868052/877d9a44e46e/fimmu-16-1494788-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b6/11868052/13517668f1fb/fimmu-16-1494788-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/28b6/11868052/877d9a44e46e/fimmu-16-1494788-g002.jpg

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本文引用的文献

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Bempedoic acid suppresses diet-induced hepatic steatosis independently of ATP-citrate lyase.贝派地酸可独立于ATP柠檬酸裂解酶抑制饮食诱导的肝脏脂肪变性。
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SSRI antidepressant citalopram reverses the Warburg effect to inhibit hepatocellular carcinoma by directly targeting GLUT1.
SSRIs 类抗抑郁药西酞普兰通过直接靶向 GLUT1 逆转沃伯格效应抑制肝癌。
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Biomarker Discovery in Liver Disease Using Untargeted Metabolomics in Plasma and Saliva.基于血浆和唾液的非靶向代谢组学在肝脏疾病中生物标志物的发现
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Hepatic stellate cells promote hepatocellular carcinoma development by regulating histone lactylation: Novel insights from single-cell RNA sequencing and spatial transcriptomics analyses.肝星状细胞通过调节组蛋白乳酰化促进肝细胞癌的发展:单细胞 RNA 测序和空间转录组学分析的新见解。
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Metabolic reprogramming and immune evasion: the interplay in the tumor microenvironment.代谢重编程与免疫逃逸:肿瘤微环境中的相互作用
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