Mitochondrial dysfunction in cancer chemoresistance

Abstract

Mitochondrial dysfunction has been associated with cancer development and progression. Recent evidences suggest that pathogenic mutations or depletion of the mitochondrial genome can contribute to development of chemoresistance in malignant tumors. In this review we will describe the current knowledge on the role of mitochondrial dysfunction in the development of chemoresistance in cancer. We will also discuss the significance of this research topic in the context of development of more effective, targeted therapeutic modalities and diagnostic strategies for cancer patients, with a particular focus on the potential use of PARP inhibitors in cancer patients displaying mitochondrial DNA mutations. We will discuss recent studies highlighting the importance of the cross-talk between the tumor microenvironment and mitochondrial functionality in determining selective response to certain chemotherapeutic drugs. Finally, owing to the similarities between cancer and yeast cell metabolism, we will point out the use of yeast as a model system to study cancer-related genes and for anti-cancer drugs screening.

Keywords: 2-Deoxyglucose (PubChem CID: 439268); 3-Bromopyruvate (PubChem CID: 70684); Cancer chemoresistance; Dichloroacetate (PubChem CID: 25975); Lonidamine (PubChem CID: 39562); Mitochondrial dysfunction; Mitochondrial retrograde signaling; Rucaparib (PubChem CID: 9931954); Tumor microenvironment; Yeast.