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. 2023 Aug 1;83(19):3192–3204. doi: 10.1158/0008-5472.CAN-23-0285

Figure 8.

Figure 8. Hypothetical working model. AR-FL transactivates SLC7A11 gene transcription by directly occupying at the promoter and enhancer regions of SLC7A11 gene. Antiandrogen treatment suppresses SLC7A11 expression and induces ferroptosis in prostate cancer cells by inhibiting AR-FL-mediated transactivation of SLC7A11 expression (left). In contrast, AR-Vs preferentially bind to the SLC7A11 gene enhancer and upregulate SLC7A11 expression, thereby conferring resistance to ferroptosis induced by ENZ treatment (right). However, the effect of AR-Vs can be abolished by CBP/p300 and BET dual inhibitor treatment-mediated inhibition of AR-V expression.

Hypothetical working model. AR-FL transactivates SLC7A11 gene transcription by directly occupying at the promoter and enhancer regions of SLC7A11 gene. Antiandrogen treatment suppresses SLC7A11 expression and induces ferroptosis in prostate cancer cells by inhibiting AR-FL-mediated transactivation of SLC7A11 expression (left). In contrast, AR-Vs preferentially bind to the SLC7A11 gene enhancer and upregulate SLC7A11 expression, thereby conferring resistance to ferroptosis induced by ENZ treatment (right). However, the effect of AR-Vs can be abolished by CBP/p300 and BET dual inhibitor treatment-mediated inhibition of AR-V expression.