Review Article

Advances in the Histone Acetylation Modification in the Oral Squamous Cell Carcinoma

Table 3

Histone acetylation sites and expression in OSCC.

SitesExpressionAcetylaseFunctionReferences

H2AK5HyperacetylationTip60Hyperacetylation is associated with cancer promotion[29]
H3K4HypoacetylationP300/Tip60Low acetylation level is positively correlated with malignancy[28]
H3K9HypoacetylationP300CSC accumulation leads to hypoacetylation and promotes tumor; its absence is a hallmark of chemoresistance[30, 31]
HyperacetylationHigh acetylation expression detected in oral cancer[29]
H3K14HyperacetylationMOZ/MORFP300-mediated hyperacetylation promotes tumor growth[29]
H3K18HyperacetylationP300High acetylation levels are associated with poor prognosis[28]
H3K27HyperacetylationGCN5Hyperacetylation enhances PD-L1 expression to promote tumor infiltration, metastasis, and recurrence[32]
HyperacetylationHyperacetylation activates PLAC2 to promote tumor proliferation[33]
H3K56HyperacetylationP300/CPBHyperacetylation is associated with cancer promotion[29]
H4K8HypoacetylationP300/CPBHypoacetylation is associated with cancer promotion[29]
H4K16HypoacetylationhMOF/Tip60Hypoacetylation is associated with cancer promotion[29]
HyperacetylationhMOF promotes acetylation to enhance oral cancer cell growth[33]