[Abstract]

To survive hostile microenvironments within tumor masses, such as nutrient deprivation, oxygen limitation, and oxidative stress which perturb mitochondrial function, tumor cells provoke an adaptive mechanism to buffer metabolic and proteotoxic stress. Different levels of quality control exist within mitochondria to detect and repair defects that affect mitochondrial performance, before the point of inescapable cell death is reached: (i) adjusting the protein-folding capacity by mitochondrial chaperones and proteases and (ii) mitochondrial dynamics allows exchange of material and promotes functional complementation and eliminates damaged mitochondria by mitophagy process. Mitochondrial stress response enables the rapid adjustment to adverse environmental conditions encountered during the dissemination process and confer survival advantage for tumor-growth, metastasis, dormant and drug-resistant cells. We seek to investigate detailed molecular mechanisms to explain how tumor cells exploits mitochondrial stress response to modulate mitochondrial functions in cancer progression.