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Androgens modify therapeutic response to cabazitaxel in models of advanced prostate cancer

Disruption of the phenotypic landscape via epithelial‐mesenchymal transition (EMT) enables prostate cancer cells to metastasize and acquire therapeutic resistance. Our previous studies demonstrated that cabazitaxel (CBZ) (second‐generation Food and Drug Administration‐approved taxane chemotherapy), used for the treatment of castration‐resistant prostate cancer (CRPC), causes reversal of EMT to mesenchymal‐epithelial transition (MET) and reduces expression of kinesin motor protein KIFC1 (HSET). The present study examined the effect of sequencing CBZ chemotherapy mediated MET on prostate tumor redifferentiation overcoming therapeutic resistance in models of advanced prostate cancer.