Acetylation and deacetylation in cancer stem-like cells

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Acetylation and deacetylation in cancer stem-like cells

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Title: Acetylation and deacetylation in cancer stem-like cells
Author: Liu, Na; Li, Shiqi; Wu, Nan; Cho, Kin-Sang

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Citation: Liu, Na, Shiqi Li, Nan Wu, and Kin-Sang Cho. 2017. “Acetylation and deacetylation in cancer stem-like cells.” Oncotarget 8 (51): 89315-89325. doi:10.18632/oncotarget.19167. http://dx.doi.org/10.18632/oncotarget.19167.
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Abstract: 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.
Published Version: doi:10.18632/oncotarget.19167
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5687692/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:34493191
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