A recent study conducted at the UW School of Veterinary Medicine has identified a molecular mechanism that enables prostate cancer cells to produce hormones that promote aggressive tumor growth, a finding that could lead to better treatments for the disease.
One current treatment uses medications or, more rarely, surgical castration to block male steroid hormones that promote prostate cancer cell growth. But the therapy becomes ineffective over time as the cancer cells begin to make their own hormones to fuel the growth. Eventually the disease develops into a deadly form called castration-resistant prostate cancer.
“It’s unclear what mechanisms make this happen,” says Joan Jorgensen, associate professor in the Department of Comparative Biosciences and member of the Class of 1993. “But we do know that a particular protein, SF1 [Steroidogenic Factor 1], regulates the synthesis of steroid hormones in normal steroid-producing tissues.”Joan Jorgsensen
This gave Jorgensen and her colleagues a focus for study. Through an analysis of cell cultures, they found that SF1 was absent in benign prostate cells and present in aggressive prostate cancer cells. In addition, when they induced the expression of SF1 in benign prostate cells, they observed steroid synthesis and cell growth, while “knockdown,” or reduced expression of SF1 in prostate cancer cells decreased steroid production and cell growth.
“This all supports the hypothesis that SF1 stimulates the abnormal formation of steroid hormones and promotes malignant tumor growth,” says Samantha Lewis, a doctoral student and lead author on the study. “It also shows a possible new target for castration-resistant prostate cancer treatment.”
The study, which appeared in Endocrinology in February 2014, was also co-authored by William Ricke, associate professor of urology in the UW School of Medicine and Public Health.
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