Figure 10. A brief overview of HSP60-ClpP–mediated UPR^mt in PCa cell survival and prostate tumor growth.

(A) HSP60 transcriptionally regulates ClpP expression via c-Myc. Two arms of mitochondrial proteostasis, mitochondrial protein folding (e.g., HSP60) and mitochondrial protease degradation (e.g., ClpP) machineries, interact and cooperate to maintain proteostasis and mitochondrial functions that lead to PCa cell survival and tumor growth. (B) Disruption of HSP60-ClpP interactions by UPR^mt inhibitor (i.e., DCEM1) deregulates mitochondrial proteostasis, mitochondrial bioenergetics, and mitohormesis, leading to PCa cell death and blockade of prostate tumor growth. Reproduced with permission from Roswell Park Comprehensive Care Center.