AKR1C3-self-employed testosterone levels could be partially attributed to redundancy in androstenedione reduction by 17-HSD3 (51) as evidenced in HCT116 AKR1C3 cells, where solitary agent treatment having a 17-HSD3 inhibitor partially prevented testosterone formation, while combination treatment having a 17-HSD3 inhibitor and SN33638 almost completely inhibited testosterone production
OnAKR1C3-self-employed testosterone levels could be partially attributed to redundancy in androstenedione reduction by 17-HSD3 (51) as evidenced in HCT116 AKR1C3 cells, where solitary agent.
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