**2. Structural features of DNA**

DNA consists of two complementary anti-parallel sugar phosphate poly-deoxyribonucleotide strands that are associated with specific hydrogen bonding between nucleotide bases. The two strands are held together primarily through Watson-Crick hydrogen bonds where A forms two hydrogen bonds with T and C forms three hydrogen bonds with G (**Figure 1**). The structure of these paired strands defines the helical grooves, within which the edges of the heterocyclic bases are exposed. The biologically relevant B-form of the DNA double helix is characterized by a shallowwide major groove and a deep-narrow minor groove. The chemical structure (feature) of the molecular surfaces in a given DNA sequence is well known in either groove. This forms the basis for molecular recognition of duplex DNA by small molecules and proteins [4, 5].

**Figure 1.** *Watson-Crick pairing between purine and pyrimidine bases in complementary DNA strand.*

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**Figure 2.**

*Anticancer Drugs' Deoxyribonucleic Acid (DNA) Interactions*

DNA as carrier of genetic information is a major target for anticancer drug interaction because of the ability to interfere with transcription and DNA replication, a major step in cell growth and division. There are three principally different ways of anticancer drug binding. First is through control of transcription factors and polymerases. Here, the anticancer drugs interact with the proteins that bind directly to DNA. Second is through RNA binding to DNA double helices to form nucleic acid triple helical structures or RNA hybridization to exposed DNA single strand regions that will be forming DNA-RNA hybrids and it may interfere with transcriptional activity. Third is through small aromatic ligand molecules that bind to DNA double helical structures through non-covalent interaction either by intercalating binder or by minor groove binders (**Figure 2**) [6, 7]. Therefore, intercalation can be defined as the process by which compounds containing planar aromatic or heteroaromatic ring systems are inserted between adjacent base pairs perpendicularly to the axis of the helix and without disturbing the overall stacking pattern due to Watson-Crick hydrogen bonding [8]. In addition, intercalation binding involves the insertion of a planar molecule between DNA base pairs, which results in a decrease in the DNA helical twist and lengthening of the DNA. While groove binding, unlike intercalation, does not induce large conformational changes in DNA and may be considered similar to standard lock-and-key models for ligand-macromolecular binding. In addition, Groove binders are usually

crescent-shaped molecules that bind to the minor groove of DNA [7].

*Groove binding to the minor groove of DNA (left) and the intercalation into DNA (right).*

In order to accommodate the binder (like intercalation binder), DNA must undergo a conformational change to create a cavity for the incoming chromophore. The double helix is therefore partially unwound, which leads to distortions of the sugar-phosphate backbone and changes in the twist angle between successive base pairs (**Figure 3**) [8]. Once the drug has been sandwiched between the DNA base

*DOI: http://dx.doi.org/10.5772/intechopen.85794*

**3. Anticancer drug-DNA interaction**
