Acetylation and deacetylation in cancer stem-like cells
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Na Liu1, Shiqi Li2, Nan Wu1 and Kin-Sang Cho3
1Department of Ophthalmology, Southwest Eye Hospital, Southwest Hospital, Third Military Medical University, Chongqing, China
2Center of biotherapy, Southwest Hospital, Third Military Medical University, Chongqing, China
3Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, Massachusetts, USA
Kin-Sang Cho, email: firstname.lastname@example.org
Nan Wu, email: email@example.com
Keywords: cancer stem cell, acetylation, deacetylation, HDAC, HAT
Received: March 14, 2017 Accepted: June 27, 2017 Published: July 11, 2017
Cancer stem-like cell (CSC) model has been established to investigate the underlying mechanisms of tumor initiation and progression. The imbalance between acetylation and deacetylation of histone or non-histone proteins, one of the important epigenetic modification processes, is closely associated with a wide variety of diseases including cancer. Acetylation and deacetylation are involved in various stemness-related signal pathways and drive the regulation of self-renewal and differentiation in normal developmental processes. Therefore, it is critical to explore their role in the maintenance of cancer stem-like cell traits. Here, we will review the extensive dysregulations of acetylation found in cancers and summarize their functional roles in sustaining CSC-like properties. Additionally, the use of deacetyltransferase inhibitors as an effective therapeutic strategy against CSCs is also discussed.
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