|
Class | Name | Target | Mechanism | References |
|
Hydroxamic acids | SAHA | HDAC I, HDAC II, HDAC IV | Induces hyperacetylation of H2A and H3 and inhibits tumor activity | [57] |
Upregulate E calcineurin and ErbB3, downregulate vimentin, EGFR and ErbB2, and enhance the antitumor effect of defibrotide | [58] |
TSA | HDAC I, HDAC II | Induced apoptosis of tumor cells in combination with PS-341 | [59] |
Combine with ATRA to inhibit tumor growth | [60] |
LBH589 | HDAC I, HDAC II, HDAC IV | Induce high acetylation of H3 and H4, inhibit tumor growth and induce apoptosis, and lead to G1 phase block | [61] |
Upregulate the expression of p21 and induce G2/M arrest and cancer cell apoptosis | [62] |
|
Cyclopeptides | Apicidin | HDAC1, HDAC3 | Competitive combination of HDAC and antitumor proliferation | [63] |
Increase the level of LC3-II and increase the apoptosis and autophagy of tumor cells | [64] |
FK228 | HDAC1, HDAC2 | Reduce Ki67 staining and inhibit tumor growth | [65] |
Induce high expression of hTERT and inhibit tumor growth | [66] |
Trapoxin | HDAC8 | Inhibit tumor cell proliferation as a potential anticancer compound | [67] |
|
Short-chain fatty acids | VPA | HDAC I, HDAC II | Promote H3, H4 acetylation and inhibit oncogene expression | [68] |
Increase G1 arrest and apoptosis of tumor cells | [69] |
PBA | HDAC I, HDAC II | Promote tumor cell apoptosis and inhibit EMT transformation | [70] |
Reduce TNF-α level and promote DNA repair | [71] |
NaBu | HDAC I, HDAC IIa | Induce cell cycle arrest, related to the increased expression of kip1 | [72] |
|
Benzamides | MS-275 | HDAC I | Make tumor cells stagnate in G0/G1 phase, enhance H3 and H4 acetylation, and promote apoptosis | [73] |
Increase cisplatin cytotoxicity | [74] |
Inhibit tumor migration and invasion by activating mir-107 and miR-138 | [75] |
MGCD0103 | HDAC I, HDAC IV | Has better radiotherapy sensitization effect | [76] |
|