Clinical Applications of HDAC Inhibitors as Anticancer Agents in Prostate, Breast, Ovarian, and Cervical Cancers

Abstract

Alongside genetic events, epigenetic processes also have a considerable impact on cancer induction and progression. Histone acetyltransferases (HATs) and histone deacetylases (HDACs) both coordinate to modulate histone modification via acetylation, an essential component of epigenetic regulation concerning gene expression. In this context, HDAC inhibition has been extensively investigated as a therapeutic approach to discovering anticancer drugs. Nevertheless, it is still highly challenging to design HDAC inhibitors (HDACis) that are successfully operational in solid tumors such as prostate, breast, ovarian, and cervical cancers. Today, some HDACis have been investigated and adopted by the U.S. Food and Drug Administration (FDA) to medically manage these malignancies, notably vorinostat, panobinostat, romidepsin, and belinostat. In addition, they promote the immune response by increasing the expression of tumor necrosis factor (TNF), interferon-gamma receptor 1 (IFN-γR1), and programmed death ligand 1 (PD-L1) in addition to other signaling pathways. A deeper comprehension of these pathways will advance our knowledge of the defects in tumor tissue while opening up opportunities for innovative and promising therapeutic strategies based on targeted cancer therapies.