Investigating Mitochondrial and Apoptosome Dysfunction 

Higher prostate cancer diagnosis and related mortality are commonly associated with African American (AA) men compared to Caucasian American (CA) men. We provide evidence that reduced level of mitochondrial DNA and reduced expression of cytochrome c contribute to mitochondrial and apoptosome dysfunction in AA patients with prostate cancer. 

Figure from a scientific research study
  • Cytochrome c-deficiency is mediated by abrogation of nuclear respiration factor-1 (Nrf1) nuclear accumulation and its binding to the cytochrome c promoter in prostate cancer. 
  • Mechanistic analysis defines that hyper-activation of c-Myc and NF-κB prevents Nrf1 nuclear translocation leading to cytochrome c-deficiency in cancer cells. 
  • Inhibition of c-Myc, NF-κB, and glycolysis promotes cytochrome c expression, caspase activation, and apoptosis in prostate cancer and tumor cells. 

Thus, restoring mitochondrial apoptosis in AA prostate cancer cells will reduce apparent racial disparity among American men with prostate cancer. 


Connect with the Chandra Lab 

Phone: 716-845-4882 

Department of Pharmacology & Therapeutics 
Roswell Park Comprehensive Cancer Center 
Elm and Carlton Streets 
Buffalo, NY 14263