Chemotherapy resistance is a rising concern in Gastric Cancer (GC) and has led to the
investigation of various cellular compounds. Α functional equilibrium of histone acetylation and
deacetylation was discovered in all cells, regulated by Histone Acetyltransferases and Deacetylases
(HDACs), controlling chromatin coiling status and changing gene expression appropriately. In accordance
with recent research, this equilibrium can be dysregulated in cancer cells aiding in the
process of carcinogenesis and tumor progression by altering histone and non-histone proteins affecting
gene expression, cell cycle control, differentiation, and apoptosis in various malignancies. In
addition, increased HDAC expression in GC cells has been associated with increased stage, tumor
invasion, nodal metastases, increased distant metastatic potential, and decreased overall survival.
HDAC inhibitors could be used as treatment regimens for GC patients and could develop important
synergistic interactions with chemotherapy drugs. The aim of this article is to review the molecular
identity and mechanism of action of HDAC inhibitors, as well as highlight their potential
utility as anti-cancer agents in GC.