Guest Speaker: Kyle Biggar, Assistant Professor, Institute of Biochemistry

Cancer is caused by unregulated cellular growth, leading to catastrophic consequences for the tissues and organs in which these cells uncontrollably multiply. Research over the past 15+ years has revealed that gene mutation and expression changes underlie the onset, progression, and therapeutic resistance of cancer. The DNA encoding these genes are packaged into a structure called chromatin, and chemical modifications to specific proteins within this structure impart regulatory information impacting the gene expression alterations that underlie cancer. These chemical modifications are termed ‘epigenetic’ as they represent a layer of regulation that is over-and-above (‘epi’) the genetic information encoded by the DNA. Importantly, mutations in regulators that control these epigenetic modification are major drivers of cancer. One of these regulators with a well-documented role in driving cancer is a lysine demethylase enzyme called KDM5C. However, the mechanism through which KDM5C regulates tumor growth and drug resistance remain unclear at this time. To help study KDM5C as a therapeutic target for cancer treatment, the Biggar lab has already developed a promising new inhibitor of this enzyme. To date, we have used this cell-active inhibitor to understand KDM5C biology in unprecedented ways. What is especially promising is that cancer cells treated with this inhibitor have displayed increased sensitivity to chemotherapy. By exploiting the strengths of both our computational, biochemical, cellular, and animal-based experimental systems, we are currently working to further develop our inhibitor to identify and functionally characterize the cancer-promoting role of KDM5C and its potential as a therapeutic cancer target. This talk will focus on the development of peptide-based drugs and their potential as a growing class of cancer therapeutics.

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