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Cellular pathway may boost prostate cancer cell growth

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University of California, Davis researchers have identified a microRNA 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, researchers say.

University of California, Davis researchers have identified a microRNA 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, researchers say.

"A number of cancer researchers are interested in microRNAs and how they are involved in diseases like leukemia," said senior author Ralph deVere White, MD. "But this is the first research to specifically look at the functional effects of microRNAs on the progression of prostate cancer."

MicroRNAs are small, single strands of RNA that regulate gene expression processes between larger strands of RNA. Working with 19 samples from the cancer center's repository of prostate cancer cells, Dr. 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.

"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," Dr. deVere White said. "This particular microRNA supports the ability of prostate cancer cells to exist and grow in its androgen-independent state."

Now having identified a cellular link between the two phases of prostate cancer, Dr. deVere White and colleagues are hopeful that miR-125b screening will at some point become a standard diagnostic tool and that genetic and chemotherapy treatments can be developed that remove this essential survival mechanism for cancer cells.

The study will be published in a future issue of the Proceedings of the National Academy of Sciences.

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