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.
Highlights
Since being proposed in 1983 [1], the theory of cancer stem-like cells (CSCs) has been gradually constructed and publicized
Bonnet and Dick first isolated CD34+CD38- cells that are capable of initiating human acute myeloid leukemia (AML)
We summarize the recent advances in the understanding of the roles of acetylation and deacetylation in CSCs, laying stress on the effect of the family of histone acetyltransferases (HATs) and Histone deacetyltransferases (HDACs) on CSCs and the potential clinical application of HDAC inhibitors to eliminate CSCs
Summary
Since being proposed in 1983 [1], the theory of cancer stem-like cells (CSCs) has been gradually constructed and publicized. According to the CSC hypothesis, tumors are organized hierarchically; the cancer cell population at the top of the hierarchy displays stem cell properties and sustains tumorigenesis. Acetylation and deacetylation influence the plasticity of chromatin structure by changing the electrical property of acetylated sites of histone and improve the stability of many non-histone proteins by covering ubiquitination sites [13]. Through these regulatory mechanisms, acetylation and deacetylation participate in the modulation of expression of various genes, which in turn modulates cellular activities like proliferation, differentiation and migration. We summarize the recent advances in the understanding of the roles of acetylation and deacetylation in CSCs, laying stress on the effect of the family of HATs and HDACs on CSCs and the potential clinical application of HDAC inhibitors to eliminate CSCs
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