Figure 5.

Schematic mechanisms of INH7 toward ER⁺ breast cancer cells. Inhibition of 17β-HSD7 by INH7 blocks E2 formation from E1 and inhibits DHT conversion into the weak estrogen metabolite (3β-diol). Furthermore, blockage of E2 conversely attenuates the expression of 17β-HSD7 itself. A decrease in E2 weakens the estrogenic effect through ER and an increase in DHT strengthens androgenic effect through AR, synergistically leading to post-receptor gene transcription culminating in cytostatic and/or cytotoxic effects.