A cancer-promoting protein’s role in the development of tumors has long been a mystery to scientists. Because aggressive tumors are more likely to become resistant to drugs and other treatments, these findings are a big step in the fight to make cancer drugs work better.
The recent discovery, made by a group of researchers led by Benjamin Myers, PhD, an investigator at the University of Utah’s Huntsman Cancer Institute and an assistant professor of oncological sciences at the U, builds on his earlier work on drug resistance. It was published today in the journal Nature Structural and Molecular Biology. Myers says, “Our findings suggest some new strategies that we might be able to use in the clinic” to improve the health of patients.
The study team looked at a protein known as Smoothened, which is crucial for the growth of healthy tissue and organs. The development and spread of brain and skin cancers, however, can be sparked when smoothened is hyperactive. Although blocking smoothened can inhibit cancer from spreading, tumors eventually develop immunity, rendering this strategy useless. Medulloblastoma is the most common brain tumor in children in the United States. Basal cell carcinoma is the most common cancer in the country, with over 3.6 million cases per year.
A signaling pathway in the body includes smoothening. From the cell surface to the interior, a signaling channel functions like a telephone cable. Instructions are sent to the cell via the messages that go along the wire.
Although we were aware of the “telephone wire,” we were unaware of how it operated. “This has created a significant gap in our capacity to therapeutically switch it off to treat cancer,” Myers claims. It is hoped that a greater understanding of it would result in cancer medications that are far more efficient.
These discoveries clarify the nature of the sent signal and how smoothened is turned on at the molecular level.
Myers claims that this discovery was greatly aided by the undergraduate biology students who worked in his lab. A special thanks goes out to postdoctoral students who were crucial to his study, as well as to John Happ, Corvin Arveseth, and Isaac Nelson, who were also important trainees. Professors Friedrich Herberg of the University of Kassel, Germany; Susan Taylor of the University of California, San Diego; and Gianluigi Veglia of the University of Minnesota are among the principal contributors.
The study was paid for by the National Institutes of Health and the Huntsman Cancer Foundation.
