期刊
CANCER SCIENCE
卷 107, 期 9, 页码 1187-1192出版社
WILEY
DOI: 10.1111/cas.13004
关键词
Cancer metabolism; chromatin; histone demethylation; lysine-specific demethylase-1; stemness
类别
资金
- JSPS KAKENHI [JP15H04707, JP15K15068, JP16K07215]
- Japan Agency for Medical Research and Development (CREST)
- Takeda Science Foundation
- Kanae Foundation for the Promotion of Medical Science
- Ono Medical Research Foundation
- Grants-in-Aid for Scientific Research [16K07215, 15K15068] Funding Source: KAKEN
Epigenetic mechanisms underlie the phenotypic plasticity of cells, while aberrant epigenetic regulation through genetic mutations and/ or misregulated expression of epigenetic factors leads to aberrant cell fate determination, which provides a foundation for oncogenic transformation. Lysine-specific demethylase-1 (LSD1, KDM1A) removes methyl groups from methylated proteins, including histone H3, and is frequently overexpressed in various types of solid tumors and hematopoietic neoplasms. While LSD1 is involved in a wide variety of normal physiological processes, including stem cell maintenance and differentiation, it is also a key player in oncogenic processes, including compromised differentiation, enhanced cell motility and metabolic reprogramming. Here, we present an overview of how LSD1 epigenetically regulates cellular plasticity through distinct molecular mechanisms in different biological contexts. Targeted inhibition of the contextdependent activities of LSD1 may provide a highly selective means to eliminate cancer cells.
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