期刊
CELLS
卷 11, 期 16, 页码 -出版社
MDPI
DOI: 10.3390/cells11162518
关键词
mitochondria; epigenetics; cancer; metabolism
类别
资金
- National Natural Science Foundation of China [81872072, 82073274]
- Science Technology Commission of Shanghai Municipality [20S11900700]
Mitochondria play a crucial role in both energy supply and regulation of key metabolites involved in epigenetic regulation. Tumorigenesis is influenced by gene mutations and the tumor microenvironment, with mitochondria and epigenetics being essential for tumor initiation, evolution, metastasis, and recurrence. Targeting mitochondrial metabolism and epigenetics holds promise for cancer treatment.
Mitochondria are not only the main energy supplier but are also the cell metabolic center regulating multiple key metaborates that play pivotal roles in epigenetics regulation. These metabolites include acetyl-CoA, alpha-ketoglutarate (alpha-KG), S-adenosyl methionine (SAM), NAD(+), and O-linked beta-N-acetylglucosamine (O-GlcNAc), which are the main substrates for DNA methylation and histone post-translation modifications, essential for gene transcriptional regulation and cell fate determination. Tumorigenesis is attributed to many factors, including gene mutations and tumor microenvironment. Mitochondria and epigenetics play essential roles in tumor initiation, evolution, metastasis, and recurrence. Targeting mitochondrial metabolism and epigenetics are promising therapeutic strategies for tumor treatment. In this review, we summarize the roles of mitochondria in key metabolites required for epigenetics modification and in cell fate regulation and discuss the current strategy in cancer therapies via targeting epigenetic modifiers and related enzymes in metabolic regulation. This review is an important contribution to the understanding of the current metabolic-epigenetic-tumorigenesis concept.
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