A paper published in the scientific journal Nature Communications by a team of Oklahoma Medical Research Foundation scientists reveals new findings about the role of a particular protein involved in the development of colon cancer.
Hong Chen, Ph.D., and her team at OMRF observed that by removing a particular type of protein called epsin, they can protect against colon cancer in experimental models. Previous work from Dr. Chen’s lab showed that epsins help regulate the formation of blood vessels, which can feed tumors in the body.
Colon cancer is the second-leading cause of cancer-related deaths in the United States and the American Cancer Society estimates that more than 90,000 new cases are reported each year.
The researchers, including the first author postdoctoral fellow, Baojun Chang, Ph.D., discovered that more epsins are present in colon cancer and, once those proteins are removed, it seems to protect against a specific process known to lead to the disease. The primary focus lies on a specific pathway called the Wnt signaling pathway, which has long been linked to colon cancer development.
“This pathway leads to cell division, and when that goes out of control you get tumor growth,” said Chen, the senior author of the new research study.
By knocking out the protein, scientists saw a decrease in tumor growth.
“In other cell studies, epsin hasn’t been found to have this particular role,” said OMRF postdoctoral fellow Kandice Tessneer, Ph.D., who collaborated on the research. “It’s new in the sense that we’ve identified a new way epsin is working, but it’s also working in such a way that it’s encouraging cancer development, which is a big deal.”
Epsins have been shown to be involved in the development of several human cancers, but their role in colon cancer is largely unknown. This research could go a long way toward answering that question.
In order to develop better drug targets, said Chen, it’s important to first understand what makes a colon cancer cell different from a normal colon cell. This discovery may impact the development of new therapeutics for colon cancer.
The work was partly supported by grants from the National Institutes of Health (RO1 HL093242, R01 HL118676, RR018758), the Oklahoma Center for the Advancement of Science and Technology and the Department of Defense.