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Histone demethylase LSD1 controls the phenotypic plasticity of cancer cells

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...

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Bibliographic Details
Published in:Cancer science 2016-09, Vol.107 (9), p.1187-1192
Main Authors: Hino, Shinjiro, Kohrogi, Kensaku, Nakao, Mitsuyoshi
Format: Article
Language:English
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Summary: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 context‐dependent activities of LSD1 may provide a highly selective means to eliminate cancer cells. LSD1, a histone demethylase, is frequently over expressed in cancer. LSD1 plays a pivotal role in regulating phenotypic plasticity in cancer cells.
ISSN:1347-9032
1349-7006
DOI:10.1111/cas.13004