Researchers at the Johns Hopkins Kimmel Cancer Center have for the first time implicated the muscle protein myosin VI in the development of prostate cancer and its spread.
In a series of lab studies with human prostate cancer cells, the Hopkins scientists were surprised to find overproduction of myosin VI in both prostate tumor cells and precancerous lesions. When the scientists genetically altered the cells to "silence" myosin VI, they discovered the cells were less able to invade in a test tube.
"Our results suggest that myosin VI may be critical in starting and maintaining the malignant properties of the majority of human prostate cancers diagnosed today," says Angelo M. De Marzo, M.D., Ph.D., a study coauthor and associate professor of pathology, urology and oncology.
The Hopkins work, published in the November issue of the American Journal of Pathology, has potential value for better ways to diagnose the disease, treat and track the effects of drugs and surgery. "Targeting myosin VI represents a promising new approach that could lead eventually new approaches to treating the disease," says Jun Luo, Ph.D., senior author of the paper and assistant professor of urology.
Myosins are a class of 40 motor proteins that power cell movement and muscle contractions. Normally, as they work, myosins slide in a single direction along the threads of a protein called actin. But myosin VI moves against the grain, and it does not function as a classical "muscle" protein.
Using a DNA microarray to study all of the genes in 59 samples of benign or cancerous prostate tissue from patients at Johns Hopkins, the researchers found the malignant samples showed a 3.7-fold higher expression of myosin VI as compared to normal samples, and a 4.6-fold increase as compared to the samples from patients with enlarged prostate.