CHAPEL HILL, N.C. Twelve years ago, UNC School of Medicine researcher Brian Strahl, PhD, found that a protein called Set2 plays a role in how yeast genes are expressed specifically how DNA gets transcribed into messenger RNA. Now his lab has found that Set2 is also a major player in DNA repair, a complicated and crucial process that can lead to the development of cancer cells if the repair goes wrong.
"We found that if Set2 is mutated, DNA repair does not properly occur" said Strahl, a professor of biochemistry and biophysics. "One consequence could be that if you have broken DNA, then loss of this enzyme could lead to downstream mutations from inefficient repair. We believe this finding helps explain why the human version of Set2 which is called SETD2 is frequently mutated in cancer."
The finding, published online June 9 in the journal Nature Communications, is the first to show Set2's role in DNA repair and paves the way for further inquiry and targeted approaches to treating cancer patients.
In previous studies, including recent genome sequencing of cancer patients, human SETD2 has been implicated in several cancer types, especially in renal cell carcinoma the most common kind of kidney cancer. SETD2 plays such a critical role in DNA transcription and repair that Strahl is now teaming up with fellow UNC Lineberger Comprehensive Cancer Center members Stephen Frye, PhD, director of the UNC Center for Integrative Chemical Biology and Drug Discovery (CICBDD), Jian Jin, PhD, also with the CICBDD, and Kim Rathmell, MD, PhD, an associate professor in the department of genetics. Their hope is to find compounds that can selectively kill cells that lack SETD2. Such personalized medicine is a goal of cancer research at UNC and elsewhere.
In recent years, scientists have discovered the importance of how DNA is packaged inside nuclei. It is now thought that the "mis-regulation" of this packaging process can trigger
|Contact: Mark Derewicz|
University of North Carolina Health Care