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代谢和表观遗传机制在肝母细胞瘤中的作用:对肿瘤生物学和治疗靶点的深入了解。

Metabolic and Epigenetic Mechanisms in Hepatoblastoma: Insights into Tumor Biology and Therapeutic Targets.

机构信息

CNRS, INSERM, Institut Necker Enfants Malades, Université Paris Cité, 75015 Paris, France.

Energy & Memory, Brain Plasticity Unit, CNRS, ESPCI Paris, PSL Research University, 75006 Paris, France.

出版信息

Genes (Basel). 2024 Oct 22;15(11):1358. doi: 10.3390/genes15111358.

DOI:10.3390/genes15111358
PMID:39596558
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11593527/
Abstract

BACKGROUND

Hepatoblastoma, the most common pediatric liver malignancy, is characterized by significant molecular heterogeneity and poor prognosis in advanced stages. Recent studies highlight the importance of metabolic reprogramming and epigenetic dysregulation in hepatoblastoma pathogenesis. This review aims to explore the metabolic alterations and epigenetic mechanisms involved in hepatoblastoma and how these processes contribute to tumor progression and survival.

METHODS

Relevant literature on metabolic reprogramming, including enhanced glycolysis, mitochondrial dysfunction, and shifts in lipid and amino acid metabolism, as well as epigenetic mechanisms like DNA methylation, histone modifications, and non-coding RNAs, was reviewed. The interplay between these pathways and their potential as therapeutic targets were examined.

RESULTS

Hepatoblastoma exhibits metabolic shifts that support tumor growth and survival, alongside epigenetic changes that regulate gene expression and promote tumor progression. These pathways are interconnected, with metabolic changes influencing the epigenetic landscape and vice versa.

CONCLUSIONS

The dynamic interplay between metabolism and epigenetics in hepatoblastoma offers promising avenues for therapeutic intervention. Future research should focus on integrating metabolic and epigenetic therapies to improve patient outcomes, addressing current gaps in knowledge to develop more effective treatments.

摘要

背景

肝母细胞瘤是最常见的小儿肝脏恶性肿瘤,其特点是分子异质性显著,晚期预后不良。最近的研究强调了代谢重编程和表观遗传失调在肝母细胞瘤发病机制中的重要性。本综述旨在探讨肝母细胞瘤中涉及的代谢改变和表观遗传机制,以及这些过程如何促进肿瘤的进展和存活。

方法

综述了代谢重编程相关文献,包括增强的糖酵解、线粒体功能障碍以及脂质和氨基酸代谢的转变,以及表观遗传机制,如 DNA 甲基化、组蛋白修饰和非编码 RNA。研究了这些途径之间的相互作用及其作为治疗靶点的潜力。

结果

肝母细胞瘤表现出支持肿瘤生长和存活的代谢转变,以及调节基因表达和促进肿瘤进展的表观遗传变化。这些途径相互关联,代谢变化影响表观遗传景观,反之亦然。

结论

肝母细胞瘤中代谢和表观遗传的动态相互作用为治疗干预提供了有前途的途径。未来的研究应侧重于整合代谢和表观遗传疗法,以改善患者的预后,解决当前知识差距,开发更有效的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0db9/11593527/63f8d759e4db/genes-15-01358-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0db9/11593527/915d79701e26/genes-15-01358-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0db9/11593527/29126efc2742/genes-15-01358-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0db9/11593527/63f8d759e4db/genes-15-01358-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0db9/11593527/915d79701e26/genes-15-01358-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0db9/11593527/29126efc2742/genes-15-01358-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0db9/11593527/63f8d759e4db/genes-15-01358-g003.jpg

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