Abstract

<p>Supplementary Figures - Figure S1 shows CC expression in AA and CA PCa cells. Figure S2 shows cell death and DEVDase activity in AA and CA PCa cells in response to docetaxel treatment. Figure S3 shows effect of CC knockdown on docetaxel-induced apoptotic cell death, caspase-3 and PARP cleavage in CA PCa cells; and mtDNA content in AA and CA PCa cells. Figure S4 shows levels of Nrf1, c-Myc, NF-κB, and PGC-1α in AA and CA PCa cells; and shows cell death, DEVDase activity, and CC expression in response to docetaxel treatment in the presence of c-Myc and NF-κB inhibitors in AA PCa cells. Figure S5 shows effect of Nrf1 knockdown on DEVDase activity in response to docetaxel treatment in the presence of c-Myc and NF-κB inhibitors or AKT activator in AA PCa cells. Figure S6 shows effect of genetic inhibition of c-Myc, NF-κB and PTEN on CC expression and DEVDase activity after docetaxel treatment in AA PCa cells. Figure S7 shows levels of p-Drp1S616 and p-Drp1S637 in primary prostate tumor (PT) and matching non-tumor (MN) tissue samples from AA and CA PCa patients. Figure S8 shows effect of Drp1 knockdown on docetaxel-induced DEVDase activity and apoptosis in CA PCa cells. Figure S9 shows knockdown of Drp1 and CC in AA PCa cells and its effect on DEVDase activity in response to docetaxel treatment in the presence of c-Myc and NF-κB inhibitors or AKT activator. Figure S10 shows expression levels of oxidative phosphorylation (OXPHOS) complexes III, IV and V in primary prostate tumor (PT) and matching non-tumor (MN) tissue samples from AA and CA PCa patients. Figure S11 shows levels of LDHA in primary prostate tumor (PT) and matching non-tumor (MN) tissue samples from AA and CA PCa patients.</p>

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