Extended Data Fig. 10: The model showing the mechanism by which ER/PR/HER2 suppress USP15-dependent stabilization of PARP1 in triple-negative breast cancer. | Nature Cancer

Extended Data Fig. 10: The model showing the mechanism by which ER/PR/HER2 suppress USP15-dependent stabilization of PARP1 in triple-negative breast cancer.

From: Loss of the receptors ER, PR and HER2 promotes USP15-dependent stabilization of PARP1 in triple-negative breast cancer

Extended Data Fig. 10: The model showing the mechanism by which ER/PR/HER2 suppress USP15-dependent stabilization of PARP1 in triple-negative breast cancer.

ER, PR and HER2 negatively regulate USP15-mediated PARP1 stabilization through different regulatory mechanisms. ER binds to the region from −2345 bp to −2341 bp in the USP15 promoter to suppress USP15 expression, PR inhibits the enzymatic activity of USP15, while HER2 abrogates the interaction between PARP1 and USP15 by competing with USP15 for binding to PARP1. Loss of ER, PR and HER2 in TNBC tissues aberrantly abolished the negative regulation of USP15-mediated PARP1 stabilization, thereby promoting the genomic stability and survival of TNBC cells.

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