The anticancer activity of benzamides is primarily attributed to their ability to interfere with cellular processes essential for cancer cell survival and proliferation. Some of the key mechanisms include:
- Inhibition of Histone Deacetylases (HDACs): Benzamides such as vorinostat and entinostat are known to inhibit HDACs, enzymes that play a crucial role in the regulation of gene expression. By inhibiting HDACs, benzamides can induce cell cycle arrest, promote apoptosis, and enhance the expression of tumor suppressor genes. - Targeting Poly (ADP-Ribose) Polymerase (PARP): Benzamides like niraparib and rucaparib act as PARP inhibitors, blocking the enzyme's role in DNA repair. This leads to the accumulation of DNA damage in cancer cells, particularly those deficient in BRCA1/2 genes, ultimately resulting in cell death. - Modulation of Dopamine Receptors: Some benzamides, such as sulpiride, are known to modulate dopamine receptors, which have been implicated in the growth and progression of certain cancers. By targeting these receptors, benzamides may inhibit cancer cell proliferation and induce apoptosis.
