Presenter Information

Courtney Fetzer, SUNY GeneseoFollow

Submission Type

Poster

Abstract

G-quadruplex (G4) DNA are non-canonical higher order structures formed from guanine rich sequences, consisting of stacked G-tetrads stabilized by non-Watson-Crick (Hoogsteen) base pairing. Early interests in G4 were spurred by the revelation that G4 is found in telomeric DNA sequences at the end of our chromosomes. These telomeric sequences were found to inhibit an enzyme overexpressed (>90%) in cancer cells, known as telomerase. Cancer cells require telomerase activity for survival and “immortality”, therefore stabilization of telomeric G4 can inhibit telomerase activity and prevent the survival of cancer cells. More recently, G4 has been shown to be overrepresented in the promoter regions of oncogenes (e.g.,c-myc and ras). As a result, G4 represents a viable target for possible anti-cancer therapeutic agents to treat previously “undruggable” targets such as thec-mycandrasoncogenes. Most traditional approaches to targeting G4 have involved using compounds with planar frameworks that are expected to either stack on top, and/or intercalate between the G4 tetrads. However, there have been reports that groove binding compounds may also target G4. These compounds would be expected to lie within the grooves typically present in the G4 structure. In this work, G4 structures formed byc-mycwere investigated by targeting it using four known duplex DNA minor groove binders (distamycin, DAPI, berenil, hoechst 33258). Using the biophysical techniques of isothermal titration calorimetry, fluorescent displacements assays and circular dichroism spectroscopy, the binding of these compounds to G4 DNA were investigated for their efficacy as an anticancer approach.

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089-Thermodynamic and Structural Studies of the Interactions between c-MYC G4 DNA and Minor Groove Binders as an Anticancer Approach

G-quadruplex (G4) DNA are non-canonical higher order structures formed from guanine rich sequences, consisting of stacked G-tetrads stabilized by non-Watson-Crick (Hoogsteen) base pairing. Early interests in G4 were spurred by the revelation that G4 is found in telomeric DNA sequences at the end of our chromosomes. These telomeric sequences were found to inhibit an enzyme overexpressed (>90%) in cancer cells, known as telomerase. Cancer cells require telomerase activity for survival and “immortality”, therefore stabilization of telomeric G4 can inhibit telomerase activity and prevent the survival of cancer cells. More recently, G4 has been shown to be overrepresented in the promoter regions of oncogenes (e.g.,c-myc and ras). As a result, G4 represents a viable target for possible anti-cancer therapeutic agents to treat previously “undruggable” targets such as thec-mycandrasoncogenes. Most traditional approaches to targeting G4 have involved using compounds with planar frameworks that are expected to either stack on top, and/or intercalate between the G4 tetrads. However, there have been reports that groove binding compounds may also target G4. These compounds would be expected to lie within the grooves typically present in the G4 structure. In this work, G4 structures formed byc-mycwere investigated by targeting it using four known duplex DNA minor groove binders (distamycin, DAPI, berenil, hoechst 33258). Using the biophysical techniques of isothermal titration calorimetry, fluorescent displacements assays and circular dichroism spectroscopy, the binding of these compounds to G4 DNA were investigated for their efficacy as an anticancer approach.

 

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