Abstract 1581: Crosstalk of androgen sensitive prostate cancer cells and insensitive prostate cancer cells

Abstract

Abstract [Background] The mechanisms that prostate cancer (PCa) progresses to castration-resistant PCa (CRPC) are adaptation and clonal selection. We hypothesized that PCa proliferated while each mechanism cooperated when PCa recurred. [Materials and Methods] After LNCaP cells were transfected with luciferase reporter driven by PSA promoter, LNCaP were cocultured with androgen-insensitive DU145 or PC-3. Then DHEA or DHT were added to the medium and luciferase assay was performed. Also, we added DHEA or DHT in the medium and measured various androgens level by LC-MS/MS. As for proliferation, LNCaP were cocultured with DU145 or PC -3 in 2-layer chamber and number of LNCaP were counted. DU145 and PC-3 were also cocultured with LNCaP cells for 4 days. We also checked migration by using 2-layer chamber and migrated cells were counted. [Results] Whereas DHEA was converted into DHT in DU145 and induced PSA promoter activity in LNCaP, the effect was not found in PC-3. Moreover, DU145 elevated DHT-induced PSA promoter activity. DU145 promoted LNCaP proliferation stimulated by DHT and DHEA, but PC-3 did not. LNCaP also promoted proliferation of DU145 and PC-3. LNCaP promoted migration of PC-3, but not DU145. [Conclusion] Cross-talk between androgen-sensitive PCa cells and androgen-insensitive PCa cells might regulate progression of CRPC. Citation Format: Yuta Takezawa, Atsushi Mizokami, Kazuaki Machioka, Kouji Izumi, Hiroaki Iwamoto, Maolake Aerken, Natsagdorg Ariunbold, Mikio Namiki. Crosstalk of androgen sensitive prostate cancer cells and insensitive prostate cancer cells. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1581.