The function of histone acetylation in cervical cancer development

Abstract

Cervical cancer is the fourth most common female cancer in the world. It is well known that cervical cancer is closely related to high-risk human papillomavirus (HPV) infection. However, epigenetics has increasingly been recognized for its role in tumorigenesis. Epigenetics refers to changes in gene expression levels based on non-gene sequence changes, primarily through transcription or translation of genes regulation, thus affecting its function and characteristics. Typical post-translational modifications (PTMs) include acetylation, propionylation, butyrylation, malonylation and succinylation, among which the acetylation modification of lysine sites has been studied more clearly so far. The acetylation modification of lysine residues in proteins is involved in many aspects of cellular life activities, including carbon metabolism, transcriptional regulation, amino acid metabolism and so on. In this review, we summarize the latest discoveries on cervical cancer development arising from the aspect of acetylation, especially histone acetylation.

Metabolites in the Tumor Microenvironment Reprogram Functions of Immune Effector Cells Through Epigenetic Modifications

“…Thus, the balance between euchromatin and heterochromatin could be tightly regulated by histone acetylation and deacetylation ( 105 , 106 ). Nonetheless, studies showed that histone acetylation/deacetylation status were dysregulated in cancer development ( 107 , 108 ), such as cervical cancer ( 109 ), breast cancer ( 110 ), leukemia ( 108 ), and non-small cell lung cancer ( 111 , 112 ). Like histone acetylation, methylation at the histone tails also regulates gene expression ( 113 , 114 ).…”

Human Papillomaviruses-Associated Cancers: An Update of Current Knowledge

“…Histone deacetylases remove acetyl residues and associate with condensed chromatin structures, which, in turn, suppress transcription [162]. Because of its significant role in cancer, HDACs became a potential target for cancer treatment [163].…”

Epigenetic Regulation of the Human Papillomavirus Life Cycle

“…Acetylation of lysine residues by HATs leads to transcriptionally active chromatin, whereas HDACs remove acetyl residues, thus marking transcriptionally repressed chromatin [43]. The HPV E6 and E7 oncoproteins promote a replication-competent environment in infected cells in part by modulating the expression and activities of HATs and HDACs [44]. The CREB-binding protein (CBP) and p300 are paralogous transcriptional coactivators with intrinsic HAT activity [45].…”