More than 80 percent of men who die from prostate cancer die with metastatic disease in their bones. But scientists know very little about how migrating prostate cancer cells set up housekeeping in bone tissue and produce the dense bony lesions characteristic of prostate cancer.
Now, new research by scientists at the University of Michigan's Comprehensive Cancer Center suggests that prostate cancer manipulates an important group of signaling proteins called Wnts (pronounced "wints") to establish itself in bone. By changing the amount and activity of Wnt proteins, prostate cancer cells upset the normal balance between formation and destruction of bony tissue.
"There is strong evidence that Wnt proteins play a central role in regulating normal skeletal development in an embryo," says Christopher L. Hall, Ph.D., a senior research fellow in urology at U-M. "But this is the first time Wnts have been shown to be involved in abnormal bone production in adult animals with prostate cancer."
Hall is first author of a paper to be published in the Sept. 1 issue of Cancer Research, which presents results from U-M studies of Wnt proteins in human prostate cancer cell lines and in laboratory mice injected with prostate cancer cells.
"Normal bone growth and remodeling depends on a controlled balance between production of new bone and resorption of existing bone," says Evan T. Keller, D.V.M., Ph.D., a professor of urology and pathology in the U-M Medical School, who directed the U-M study. "When a tumor forms in bone, it upsets this balance."
Several types of cancer metastasize to bone, according to Keller, but most of them tip the balance toward destruction producing what scientists call osteolytic lesions, or holes in the bone. Prostate
Contact: Sally Pobojewski
University of Michigan Health System