Figure 6.

Schematic diagram of the molecular mechanism on mifepristone in inhibiting HCC cell growth. This figure illustrates the roles of GR, HSP60, and survivin in HCC cells in the presence and absence of mifepristone, showcasing the molecular mechanism behind its inhibitory effects. (A) Under normal physiological conditions, HSP60-GR and HSP60-survivin complexes are localized in the cytosol. HSP60 binds to survivin, thereby stabilizing survivin for cell survival. (B) In the presence of mifepristone, it not only binds to GR but also reduces the activity of ΔΨm, leading to the release of HSP60 from mitochondria to the cytosol (steps 1 to 2). The accumulation of cytosolic HSP60 enhances the formation of HSP60-survivin complexes, facilitating interaction with GR (steps 3 to 5). Subsequently, survivin is degraded through the ubiquitin-proteasome pathway (UPP) (step 6). Ultimately, this process results in decreased cell proliferation and increased apoptosis (step 7).