A collaborative team of interdisciplinary researchers led by Dr. Ryan P. Hobbs, PhD, a postdoctoral fellow at John Hopkins Bloomberg School of Public Health’s Department of Biochemistry and Molecular Biology, recently revealed study findings suggesting a protein known as keratin 17, a clinical biomarker for many types of cancers, may also play a significant role in tumor growth. The findings from the study, entitled, “Keratin-dependent regulation of Aire and gene expression in skin tumor keratinocytes,” were published in the latest edition of Nature Genetics.
In a University press release, Dr. Hobbs explained the importance of the findings, “Keratin 17 is a sensitive marker for various cancers and several other acute and chronic diseases affecting the skin, but we didn’t know whether it was a driver of the disease or just an innocent bystander. We didn’t know if the keratin was actually involved in the onset and promotion of skin tumors or if it was just along for the ride. This research, focused on models for cancer affecting the skin, tells us it’s more of a driver than a passenger. A better understanding of what drives the onset, growth and characteristics of tumors will ultimately help us develop better biomarkers and treatments”
Dr. Hobbs and his team used mice that were genetically engineered to have the most common form of skin cancer, viral HPV-induced squamous cell carcinoma. They studied mice with normal keratin 17 levels and those in which the protein was absent, and compared tumor growth rates between the two groups of animals.
The results showed that mice without keratin 17 had significantly lower tumor growth rates, accompanied by a lowered immune and inflammatory response, when compared to the animals in which the protein was physiologically intact. This most likely means that keratin 17 is not responsible for inducing cancer, but that the immune and inflammatory response it initiates increases the rate of tumor growth.
As explained by Dr. Pierre A. Coulombe, PhD, E.V. McCollum professor and chair of the Bloomberg School’s Department of Biochemistry and Molecular Biology and senior study author, “Keratin 17 is like a throttle pedal. It drives a specific type of sustained inflammation that helps a cancer become a cancer.”
The discovery of the role of keratin 17 in tumor growth is important for future anti-cancer drug development with the purpose of delaying tumor formation, so that both the patient’s immune system and cancer treatment therapies can be more successful in killing the already present tumor cells.