Pioneering New Drug Targets for Inhibiting c-Myc Expression


Robert Brown, Quinea Lassiter, Caleb Sutherland


Laurence Hurley, Laurence Hurley, PhD, Professor Howard J. Schaeffer Endowed Chair in Pharmaceutical Sciences Director, BIO5 Oro Valley Member, The University of Arizona

The c-Myc oncogene is deregulated in about 80% of all human cancers. The overexpression of the c-Myc gene in various types of cancers is responsible for initiating cell proliferation, metastasis, and tumor growth. The overarching aim of this research is to discover drug compounds that will interact specifically with the c-Myc i-Motif structure and inhibit c-Myc gene expression in Burkitt’s lymphoma. The FRET i-Motif assay identified two compounds NSC 316157 and NSC 260594 from the NCI drug library as potential i-Motif stabilizers. Circular Dichroitic studies indicate that at 2 molar equivalents NSC 316157 and NSC 260954 destabilize the i-Motif to a significant extent. Gene expression analysis by quantitative Real Time PCR reveals compound NSC 316157 decreases c-Myc expression by 80%. These results suggest that NSC 316157 inhibits c-Myc expression in Burkitt’s lymphoma by targeted destabilization of the c-Myc i-Motif.

Presented by:


Saturday, November 23, 2013




Poster Session 2 - Villalobos Hall

Presentation Type:

Poster Presentation