The progression of prostate cancer (PCa) mainly occurs caused by androgens. There is a link

between intratumoral steroidogenesis and castration-resistant prostate cancer. This study
aimed to determine the mRNA expression of various steroidogenic enzymes (CYP17A1,
CYP11A1, CYP19A1, HSD3B1, and AKR1C2) in metastatic and non-metastatic prostate
cancer patients. This study was conducted at the Anatomical Pathology Laboratory and
Urologi Division, Department of Surgery, Faculty of Medicine, Public Health and Nursing,
Universitas Gadjah Mada/Dr. Sardjito General Hospital, Yogyakarta from September-
November 2017. Samples were taken from 30 paraffin blocks with adenocarcinoma of
prostate, stained with hematoxylin-eosin (HE) and then classified into metastatic and nonmetastatic
groups. Samples then underwent deparaffinization procedure and examination
of mRNA expression of CYP17A1, CYP11A1, CYP19A1, HSD3B1, AKR1C2 genes using
Real-Time PCR. The mean mRNA expressions of CYP11A1, CYP17A1, CYP19A1,
HSD3B1, and AKR1C2 genes in the metastatic adenocarcinoma prostate group were 7.08,
10.11, 3.94, 4.84 and 3.58, respectively. In the non-metastatic group, the mean mRNA
expressions of CYP11A1, CYP17A1, CYP19A1, HSD3B1, and AKR1C2 genes were 4.62,
9.45, 3.46, 2.68 and 4.92, respectively. The mean of mRNA expression of CYP11A1,
CYP17A1, CYP19A1, and HSD3B1 genes were higher in the metastatic group than nonmetastatic
adenocarcinoma prostate group. However, it was not statistically significant
(p>0.05). The highest mRNA expression of steroidogenic enzymes was the CYP17A1
gene. In conclusion, the mRNA expressions of CYP17A1, CYP11A1, CYP19A1, HSD3B1
were higher in the metastatic prostate cancer patients compared to that in non-metastatic
prostate cancer patients but statistically not significant.

R. Umbas et al., “Panduan Penatalaksanaan Kanker Prostat 2011,” 2011. [2] T. Chandrasekar, J. C. Yang, A. C. Gao, and C. P. Evans, “Targeting molecular resistance in castration-resistant prostate cancer,” BMC Med., vol. 13, no. 1, p. 206, 2015. [3] T. W. Friedlander et al., “Common structural and epigenetic changes in the genome of castration-resistant prostate cancer,” Cancer Res., vol. 72, no. 3, pp. 616–625, 2012. [4] S. J. Hotte and F. Saad, “Current management of castrate-resistant prostate cancer,” Curr. Oncol., vol. 17, no. SUPPL. 2, pp. 72–79, 2010. [5] E. A. Mostaghel and P. S. Nelson, “Intracrine androgen metabolism in prostate cancer progression: mechanisms of castration resistance and therapeutic implications,” Best Pract. Res. Clin. Endocrinol. Metab., vol. 22, no. 2, pp. 243–258, 2008. [6] M. Knuuttila and M. Knuuttila, ANDROGEN BIOSYNTHESIS IN PROSTATE CANCER : Evidence from preclinical models and clinical specimens ANDROGEN BIOSYNTHESIS IN PROSTATE CANCER : 2017. [7] W. L. Miller, “Steroidogenic Enzymes,” vol. 13, pp. 1–18, 2008. [8] W. L. Miller and R. J. Auchus, “The molecular biology, biochemistry, and physiology of human steroidogenesis and its disorders,” Endocr. Rev., vol. 32, no. 1, pp. 81–151, 2011. [9] S. M. Green, E. A. Mostaghel, and P. S. Nelson, “Androgen action and metabolism in prostate cancer,” Mol. Cell. Endocrinol., vol. 360, no. 1–2, pp. 3–13, 2012. [10] N. M. F. S. A. Cerqueira et al., “Cholesterol Biosynthesis: A Mechanistic Overview,” Biochemistry, vol. 55, no. 39, pp. 5483–5506, 2016. [11] W. L. Miller, “Androgen biosynthesis from cholesterol to DHEA,” Mol. Cell. Endocrinol., vol. 198, no. 1–2, pp. 7–14, 2002. [12] S. Salvi et al., “Circulating cell-free AR and CYP17A1 copy number variations may associate with outcome of metastatic castration-resistant prostate cancer patients treated with abiraterone,” Br. J. Cancer, vol. 112, no. 10, pp. 1717–1724, 2015. [13] R. J. Santen, G. R. Petroni, M. J. Fisch, C. E. Myers, D. Theodorescu, and R. B. Cohen, “Use of the aromatase inhibitor anastrozole in the treatment of patients with advanced prostate carcinoma.,” Cancer, vol. 92, no. 8, pp. 2095–2101, 2001. [14] D. R. Tobergte and S. Curtis, Drug Management of prostate cancer ., vol. 53, no. 9. 2013. [15] Q. Ji, L. Chang, D. VanDenBerg, F. Z. Stanczyk, and A. Stolz, “Selective reduction of AKR1C2 in prostate cancer and its role in DHT metabolism,” Prostate, vol. 54, no. 4, pp. 275–289, 2003.