UC Davis researchers identify a cellular pathway that makes prostate ca...( (SACRAMENTO Calif.) Expanding evide...),Health

(SACRAMENTO, Calif.) Expanding evidence that tiny strands of RNA called microRNAs play big roles in the progress of some cancers, UC Davis researchers have identified one that helps jump start prostate cancer cell growth midway through the disease process, eventually causing it to become fatal. The discovery is an important link to finding new treatments targeting this cellular function and reducing cancer deaths among American men.

A number of cancer researchers are interested in microRNAs and how they are involved in diseases like leukemia, said Ralph deVere White, director of the UC Davis Cancer Center, professor of urology and senior author on the study. But this is the first research to specifically look at the functional effects of microRNAs on the progression of prostate cancer.

Relatively new discoveries in genetic research, microRNAs are small, single strands of RNA that regulate gene expression processes between larger strands of RNA. Working with 19 samples from the cancer centers repository of prostate cancer cells, deVere White and his team used high-resolution analysis techniques to identify microRNAs that were differentially expressed. Of five that were distinct, one miR-125b caught their attention because of its presence at high levels in both androgen-dependent and androgen-independent prostate cancer cells. Androgens, such as testosterone, are known to promote tumor growth. While androgen suppression treatments slow the progress of prostate cancer, they do not cure it.

One of the most confounding things about prostate cancer is that after a period of success with androgen suppression therapy, the cancer starts to thrive again, deVere White explained. Thats when the disease becomes fatal. This particular microRNA supports the ability of prostate cancer cells to exist and grow in its androgen-independent state. And we currently have no effective treatments for the androgen-independent state of the disease.