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Effect of Steroid 5α-Reductase Inhibitors on Markers of Tumor Regression and Proliferation in Prostate Cancer

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Androgen Action in Prostate Cancer

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Abstract

Intracrine conversion of testosterone to the more potent dihydrotestosterone (DHT) by the enzymes 5α-reductase type 1 (5αR1) and type 2 (5αR2) is important for normal and pathological growth of the prostate. Consequently, inhibitors of 5αR have been developed to treat prostate disease. Finasteride, the first commercially available 5αR inhibitor, targets 5αR2 since this isoenzyme predominates in benign prostate tissue. Finasteride has been shown to cause a 20–30% reduction in prostate volume in men with BPH, through a combination of atrophy and apoptosis. It has further been shown to reduce the incidence of detectable prostate cancer by 25% in the Prostate Cancer Prevention Trial (PCPT), through prevention and/or treatment of subclinical carcinomas. However, development of prostate cancer is accompanied by a decrease in 5αR2 levels and an increase in 5αR1. The dual 5αR inhibitor dutasteride provides greater suppression of DHT formation than finasteride (93–97% vs. 68–86%) and may be even more effective in prevention of prostate cancer. The 4-year Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial is currently underway to test this hypothesis. Defining the role of 5αR inhibitors in treatment of established prostate cancer requires further investigation. However, the effect of such inhibitors on markers of tumor regression (apoptosis, proliferation, angiogenesis, and tumor histopathology) has been explored, in part. In several studies of men with BPH, who were treated with finasteride for 3 months to 4 years and who subsequently developed prostate cancer, the effect of finasteride on the histopathology of malignant cells was unclear. Atrophic changes such as pyknosis and vacuolization were reported in some studies, and no significant effect of finasteride was observed in others. Finasteride was not shown to have an effect on prostate cancer cell proliferation. Its effect on apoptosis and angiogenesis in prostate cancer has not been studied. In contrast, the dual 5αR inhibitor dutasteride has been shown to cause significant regressive changes in established prostate cancer, although some of the effect is time dependent. Short-term treatment (6–10 weeks) caused a 40% reduction in tumor volume and resulted in significant increases in apoptosis, number of atrophic glands, and stromal:epithelial ratio. It was also associated with a nonsignificant decrease in microvessel density. After longer treatment (4 months), the regressive changes induced by dutasteride waned, although reductions in tumor volume continued to be evident. In summary, the results from the PCPT demonstrated that inhibition of 5αR may prevent or delay prostate cancer in some patients. From preprostatectomy trials of dutasteride, it is also clear that suppression of DHT formation with a 5αR inhibitor may cause regression of prostatic carcinomas. The fact that regressive changes were not observed to the same extent with finasteride may be for two reasons. First, since finasteride is a 5αR2 selective inhibitor, DHT formation can continue due to the action of 5αR1. Second, the timing of the observations in many of the studies with finasteride may not have been optimal.

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  1. Department of Biochemistry and Molecular Biology, Dalhousie University, 9D Sir Charles Tupper Building, Halifx, NS, Canada, B3H 1X5

    Lynn N. Thomas & Roger S. Rittmaster

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Thomas, L.N., Rittmaster, R.S. (2009). Effect of Steroid 5α-Reductase Inhibitors on Markers of Tumor Regression and Proliferation in Prostate Cancer. In: Mohler, J., Tindall, D. (eds) Androgen Action in Prostate Cancer. Springer, New York, NY. https://doi.org/10.1007/978-0-387-69179-4_7

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