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Frontiers in Bioscience-Scholar (FBS) is published by IMR Press from Volume 13 Issue 1 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

1 Jan 2017Review

Mitochondrial dysfunction and prostate cancer racial disparities among American men

Ajay K. Chaudhary 1, Jordan O’Malley 1, Sandeep Kumar 1, Joseph R. Inigo 1, Rahul Kumar 1, Neelu Yadav 1, Dhyan Chandra 1,*
Affiliation
Article Info

1 Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, New York, USA

*Author to whom correspondence should be addressed.

 

Abstract

The gap between prostate cancer disparities among American men is narrowing, which is mostly due to increased screening of African American (AA) men. However, the biological reasons for prostate cancer disparities among American men still remain undefined. Mitochondrion, an organelle within cells, regulates both cell survival and cell death mechanisms. These cellular signaling pathways require various proteins localized to mitochondria, which are encoded by both nuclear DNA (nDNA) and mitochondrial DNA (mtDNA). Interestingly, prostate tissues from AA men harbor reduced mtDNA content compared to Caucasian American (CA) men. Therefore, changes in mitochondrial genes may have detrimental consequences in terms of cellular signaling regulated by mitochondria in AA men. This review describes the plausible underlying mechanism of mtDNA depletion and its impact in driving resistance to therapy leading to faster progression and poor prognosis in African American men with prostate cancer. Since defective cellular signaling is critical for prostate cancer cell survival, restoring mitochondrial function may provide strategies to alleviate prostate cancer disparities among American men.

Keywords

  • Prostate Cancer Racial Disparity
  • Mitochondrial Dysfunction
  • Oxidative Phosphorylation
  • OXPHOS
  • Apoptosis
  • Mitochondrial Dna
  • mtDNA
  • Review

References