Abstract
Histone deacetylases (HDACs) play an important role in regulating target gene expression. They have been highlighted as a novel category of anticancer targets, and their inhibition can induce apoptosis, differentiation, and growth arrest in cancer cells. In view of the fact that HDAC inhibitors and other antitumor agents, such as BET inhibitors, topoisomerase inhibitors, and RTK pathway inhibitors, exert a synergistic effect on cellular processes in cancer cells, the combined inhibition of two targets is regarded as a rational strategy to improve the effectiveness of these single-target drugs for cancer treatment. In this review, we discuss the theoretical basis for designing HDAC-involved dual-target drugs and provide insight into the structure-activity relationships of these dual-target agents.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Antineoplastic Agents / chemistry*
-
Antineoplastic Agents / pharmacology
-
Antineoplastic Agents / therapeutic use
-
DNA Damage / drug effects
-
Histone Deacetylase Inhibitors / chemistry*
-
Histone Deacetylase Inhibitors / pharmacology
-
Histone Deacetylase Inhibitors / therapeutic use
-
Histone Deacetylases / chemistry
-
Histone Deacetylases / metabolism*
-
Humans
-
Neoplasms / drug therapy
-
Protein Kinases / chemistry
-
Protein Kinases / metabolism
-
Protein Kinases / pharmacology
-
Proteins / antagonists & inhibitors
-
Proteins / metabolism
-
Structure-Activity Relationship
-
Topoisomerase Inhibitors / chemistry
-
Topoisomerase Inhibitors / pharmacology
-
Topoisomerase Inhibitors / therapeutic use
Substances
-
Antineoplastic Agents
-
Histone Deacetylase Inhibitors
-
Proteins
-
Topoisomerase Inhibitors
-
bromodomain and extra-terminal domain protein, human
-
Protein Kinases
-
Histone Deacetylases