Implications of Therapy-Induced Selective Autophagy on Tumor Metabolism and Survival

Figure 2

Mitophagy, nucleophagy, and ubiquitin-mediated autophagy are associated with cell survival or cell death depending on the level of activation. A homeostatic level of mitophagy promotes cell survival by liberating nutrients and by clearing dysfunctional mitochondria that signal for apoptosis. Conversely, hyperactivation of mitophagy can lead to a loss in the cell’s ability to generate ATP, resulting in cell death. Similarly, a homeostatic level of nucleophagy protects cells against the accumulation of structural damage to the nucleus and may provide energetic and biosynthetic resources that aid in repair. Nucleophagy also appears to be associated with cell death in specialized cell types facing extreme stress. Ubiquitin-mediated autophagy appears to function solely as a survival pathway that clears misfolded protein aggregates and liberates metabolites that may be used for energy production.