文献检索文档翻译深度研究
Suppr Zotero 插件Zotero 插件
邀请有礼套餐&价格历史记录

新学期,新优惠

限时优惠:9月1日-9月22日

30天高级会员仅需29元

1天体验卡首发特惠仅需5.99元

了解详情
不再提醒
插件&应用
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
高级版
套餐订阅购买积分包
AI 工具
文献检索文档翻译深度研究
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2025

癌症中的代谢重编程和表观遗传修饰:从影响和机制到治疗潜力。

Metabolic reprogramming and epigenetic modifications in cancer: from the impacts and mechanisms to the treatment potential.

机构信息

Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, 410013, Hunan, China.

University of South China, Hengyang, 421001, Hunan, China.

出版信息

Exp Mol Med. 2023 Jul;55(7):1357-1370. doi: 10.1038/s12276-023-01020-1. Epub 2023 Jul 3.


DOI:10.1038/s12276-023-01020-1
PMID:37394582
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10394076/
Abstract

Metabolic reprogramming and epigenetic modifications are hallmarks of cancer cells. In cancer cells, metabolic pathway activity varies during tumorigenesis and cancer progression, indicating regulated metabolic plasticity. Metabolic changes are often closely related to epigenetic changes, such as alterations in the expression or activity of epigenetically modified enzymes, which may exert a direct or an indirect influence on cellular metabolism. Therefore, exploring the mechanisms underlying epigenetic modifications regulating the reprogramming of tumor cell metabolism is important for further understanding tumor pathogenesis. Here, we mainly focus on the latest studies on epigenetic modifications related to cancer cell metabolism regulations, including changes in glucose, lipid and amino acid metabolism in the cancer context, and then emphasize the mechanisms related to tumor cell epigenetic modifications. Specifically, we discuss the role played by DNA methylation, chromatin remodeling, noncoding RNAs and histone lactylation in tumor growth and progression. Finally, we summarize the prospects of potential cancer therapeutic strategies based on metabolic reprogramming and epigenetic changes in tumor cells.

摘要

代谢重编程和表观遗传修饰是癌细胞的标志。在癌细胞中,代谢途径的活性在肿瘤发生和癌症进展过程中发生变化,表明代谢具有调节的可塑性。代谢变化通常与表观遗传变化密切相关,例如表观遗传修饰酶的表达或活性的改变,这些改变可能对细胞代谢产生直接或间接的影响。因此,探索表观遗传修饰调节肿瘤细胞代谢重编程的机制对于进一步了解肿瘤发病机制非常重要。在这里,我们主要关注与癌症细胞代谢调控相关的表观遗传修饰的最新研究,包括在癌症背景下葡萄糖、脂质和氨基酸代谢的变化,然后强调与肿瘤细胞表观遗传修饰相关的机制。具体来说,我们讨论了 DNA 甲基化、染色质重塑、非编码 RNA 和组蛋白乳酸化在肿瘤生长和进展中的作用。最后,我们总结了基于肿瘤细胞代谢重编程和表观遗传变化的潜在癌症治疗策略的前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da4/10394076/9101931ae610/12276_2023_1020_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da4/10394076/8eeadc447424/12276_2023_1020_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da4/10394076/7d63d1c0f24e/12276_2023_1020_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da4/10394076/1726f9ca4dc7/12276_2023_1020_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da4/10394076/9101931ae610/12276_2023_1020_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da4/10394076/8eeadc447424/12276_2023_1020_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da4/10394076/7d63d1c0f24e/12276_2023_1020_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da4/10394076/1726f9ca4dc7/12276_2023_1020_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8da4/10394076/9101931ae610/12276_2023_1020_Fig4_HTML.jpg

相似文献

[1]
Metabolic reprogramming and epigenetic modifications in cancer: from the impacts and mechanisms to the treatment potential.

Exp Mol Med. 2023-7

[2]
Metabolic reprogramming and epigenetic modifications on the path to cancer.

Protein Cell. 2022-12

[3]
Molecular Pathways: Metabolic Control of Histone Methylation and Gene Expression in Cancer.

Clin Cancer Res. 2017-8-1

[4]
Crosstalk between metabolic reprogramming and epigenetics in cancer: updates on mechanisms and therapeutic opportunities.

Cancer Commun (Lond). 2022-11

[5]
Effect of non-enzymatic glycosylation in the epigenetics of cancer.

Semin Cancer Biol. 2022-8

[6]
Lactate-induced protein lactylation: A bridge between epigenetics and metabolic reprogramming in cancer.

Cell Prolif. 2023-10

[7]
Epigenetic drugs as pleiotropic agents in cancer treatment: biomolecular aspects and clinical applications.

J Cell Physiol. 2007-8

[8]
Rewriting cellular fate: epigenetic interventions in obesity and cellular programming.

Mol Med. 2024-10-10

[9]
The role of histone modifications in epigenetic transitions during normal and perturbed development.

Ernst Schering Res Found Workshop. 2006

[10]
Epigenetic alterations in cancer.

Front Biosci (Landmark Ed). 2020-3-1

引用本文的文献

[1]
Effects of different exercise prescription parameters on metabolic and inflammatory biomarkers in cancer patients: a systematic review, meta-analysis, and meta-regression.

Front Immunol. 2025-8-14

[2]
NeuroD1 drives a KAT2A-FDFT1 signaling axis to promote cholesterol biosynthesis and hepatocellular carcinoma progression via histone H3K27 acetylation.

Oncogene. 2025-9-1

[3]
Metastatic breast cancer cells are vulnerable to fatty acid oxidation inhibition through DDX3-DRP1-mediated mitochondrial plasticity.

Redox Biol. 2025-8-26

[4]
Targeting epigenetic modifications as an emerging immunotherapeutic strategy for cancers.

Immunol Res. 2025-8-19

[5]
Ferroptosis as a therapeutic target in glioblastoma: Mechanisms and emerging strategies.

Mol Ther Nucleic Acids. 2025-7-30

[6]
DHCR24 overexpression is involved in lipid metabolic reprogramming to drive cervical cancer malignant progression and is associated with immune microenvironment.

BMC Cancer. 2025-8-9

[7]
Melatonin: a natural guardian in cancer treatment.

Front Pharmacol. 2025-7-18

[8]
Untargeted metabolomics analysis of serum metabolic signatures as novel biomarkers for gastric carcinoma.

World J Clin Oncol. 2025-7-24

[9]
A novel defined manganese metabolism-related gene signature for predicting the prognosis of pancreatic ductal adenocarcinoma.

Oncol Lett. 2025-7-9

[10]
Long interspersed nuclear element 1 methylation in non-small cell lung cancer: implications for diagnosis, prognosis, and therapeutic targeting.

Cell Commun Signal. 2025-7-22

本文引用的文献

[1]
Structural insights into adhesion GPCR ADGRL3 activation and G, G, G, and G coupling.

Mol Cell. 2022-11-17

[2]
The FUS/circEZH2/KLF5/ feedback loop contributes to CXCR4-induced liver metastasis of breast cancer by enhancing epithelial-mesenchymal transition.

Mol Cancer. 2022-10-12

[3]
Positron Emission Tomography/Computed Tomography in Thyroid Cancer.

PET Clin. 2022-4

[4]
MiR-601 Promotes Cell Proliferation of Human Glioblastoma Cells by Suppressing TINP1 Expression.

Altern Ther Health Med. 2022-2

[5]
Downregulation of SLC27A6 by DNA Hypermethylation Promotes Proliferation but Suppresses Metastasis of Nasopharyngeal Carcinoma Through Modulating Lipid Metabolism.

Front Oncol. 2022-1-3

[6]
CircRPN2 Inhibits Aerobic Glycolysis and Metastasis in Hepatocellular Carcinoma.

Cancer Res. 2022-3-15

[7]
MiR-378a inhibits glucose metabolism by suppressing GLUT1 in prostate cancer.

Oncogene. 2022-3

[8]
Hallmarks of Cancer: New Dimensions.

Cancer Discov. 2022-1

[9]
The cholesterol pathway: impact on immunity and cancer.

Trends Immunol. 2022-1

[10]
F FDG imaging - response criteria in tumors.

Eur J Radiol. 2022-2

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

推荐工具

医学文档翻译智能文献检索