串扰
表观遗传学
重编程
胰腺癌
癌变
生物
转移
癌症研究
后生
肿瘤微环境
生物信息学
遗传学
癌症
DNA甲基化
基因
细胞
基因表达
肿瘤细胞
物理
光学
作者
Jie Ren,Bo Ren,Xiaohong Liu,Ming Cui,Yuan Fang,Xing Wang,Feihan Zhou,Minzhi Gu,Ruiling Xiao,Jialu Bai,Lei You,Yupei Zhao
出处
期刊:Cancer Letters
[Elsevier]
日期:2024-02-02
卷期号:587: 216649-216649
被引量:14
标识
DOI:10.1016/j.canlet.2024.216649
摘要
Pancreatic cancer is a highly malignant solid tumor with a poor prognosis and a high mortality rate. Thus, exploring the mechanisms underlying the development and progression of pancreatic cancer is critical for identifying targets for diagnosis and treatment. Two important hallmarks of cancer—metabolic remodeling and epigenetic reprogramming—are interconnected and closely linked to regulate one another, creating a complex interaction landscape that is implicated in tumorigenesis, invasive metastasis, and immune escape. For example, metabolites can be involved in the regulation of epigenetic enzymes as substrates or cofactors, and alterations in epigenetic modifications can in turn regulate the expression of metabolic enzymes. The crosstalk between metabolic remodeling and epigenetic reprogramming in pancreatic cancer has gained considerable attention. Here, we review the emerging data with a focus on the reciprocal regulation of metabolic remodeling and epigenetic reprogramming. We aim to highlight how these mechanisms could be applied to develop better therapeutic strategies.
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