Investigators at the University of North Carolina say they have nailed down some solid preclinical evidence to suggest that the Dicer enzyme could be a good target for developers looking to advance new treatments for brain cancer.
Building on earlier work that established Dicer's role in repairing the DNA damage that can occur among rapidly dividing cells, the team at UNC used an animal model for medulloblastoma--a common brain cancer among children--to explore how blocking the enzyme might influence the disease.
They concluded that blocking the repair mechanism not only accelerated the damage and spurred cell death, it also appeared to make the remaining tumors smaller with cells that are more vulnerable to chemotherapy. Their results were published in the journal Cell Reports.
"We found that cancerous cells upregulate Dicer," said Vijay Swahari, a postdoctoral fellow at the UNC Neuroscience Center and the first author of this study. "We think tumors upregulate Dicer because its function is to repair DNA."
Swahari and his colleagues say that their work helps establish a new target for drug developers to focus on.
"This is the first time that the specific function of Dicer for DNA damage has been looked at in the context of the developing brain or even in brain tumors, despite that the fact that the protein has been extensively studied," said Mohanish Deshmukh, a UNC Lineberger member and professor in the UNC School of Medicine Department of Cell Biology and Physiology and also the Neuroscience Center. "We have found that targeting Dicer could be an effective therapy to either prevent cancer development or to actually sensitize tumors to chemotherapy."