Interaction of anthraquinone anti-cancer drugs with DNA
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DNA is a primary target for drugs in the cell. The mode of action of many chemotherapeutic agents is thought to be due to their ability to intercalate between double helix DNA base pairs. Atraquinones are generally thought to exert their biological actions through binding with DNA followed by an interference with DNA replication, transcription, and inhibition of gene expression. The design of small drug molecules that selectively target DNA, with high binding affinities, has led to the discovery of many anticancer, antibiotic, and antiviral drugs. Most DNA-targeted molecules start their bindin...
DNA is a primary target for drugs in the cell. The mode of action of many chemotherapeutic agents is thought to be due to their ability to intercalate between double helix DNA base pairs. Atraquinones are generally thought to exert their biological actions through binding with DNA followed by an interference with DNA replication, transcription, and inhibition of gene expression. The design of small drug molecules that selectively target DNA, with high binding affinities, has led to the discovery of many anticancer, antibiotic, and antiviral drugs. Most DNA-targeted molecules start their binding with double helix DNA non-covalently which subsequently may developed to covalent binding. Non-covalent binding may include pi- stacking, hydrogen bonding, electrostatic, charge transfer, and hydrophobic interactions. All these interactions may contribute to the drug/DNA interaction mechanism so that the main objective of this study is to explore the dominant interaction. This information is crucial for design and development of new drugs.
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