Table 4.
Application of DNMTi and HDACi to OC treatment
| Drugs | Function | Reference |
|---|---|---|
| DNMTi | ||
| SGI-110 | 1. Drug sensitizer used in combination with cisplatin | [156] |
| 2. Enhances the immune recognition of tumor cells by regulating MHC class I and immunomodulatory molecules in EOC cells, and is superior to AZA or DAC | [157] | |
| 5-Aza-2’-deoxycytidine (5-AZA-CdR) | Upregulate endogenous retrovirus (ERV) with G9Ai, synergistically induce antitumor | [158] |
| 5-Azacytidine (5AZA-C) | Induced the recruitment of activated (IFNγ+) CD4+T cells, CD8+ T cells and NK cells combining with α-difluoromethylornithine (DFMO) | [159] |
| HDACi | ||
| Entinostat (class I HDACi) | Synergistic effect with cisplatin in HGSOC | [160] |
| Vorinostat | Inhibit tumor growth and prolong survival via targeting CD146 | [161] |
| Panobinostat | 1. Synergistic effect with carboplatin in EOC | [162] |
| 2. Reduce homologous recombination (HR) cyclin E-overexpression, as a means of enhancing PARPi activity | [163] | |
| Thailandepsins | Inhibit cell viability and induce apoptosis | [164] |
| Suberoylanilide hydroxamic acid (SAHA) | Combined olaparib induced apoptosis and pH2AX expression more strongly to a greater extent than either drug alone | [165] |