|
Drug | Effect | Role of ROS | Source of oxidative stress | Ref. |
|
Sorafenib | Apoptosis and prosurvival autophagy | Dose-dependent cytostatic and cytotoxic effects; apoptotic cell death | Mitochondrial ROS and GSH depletion | [70, 71] |
Oxaliplatin | Apoptosis and prosurvival autophagy | Enhanced apoptotic cell death upon autophagy inhibition | Inhibition of thioredoxin reductase | [76, 92] |
Salinomycin | Apoptosis and inhibition of autophagy | Contribution to apoptosis activation | Accumulation of dysfunctional mitochondria due to impaired autophagic flux | [79] |
Capsaicin | Apoptosis and induction of cytoprotective STAT3-dependent autophagy | Phosphorylation of STAT3 and activation of autophagy | Inhibition of mitochondrial complexes I and III; reduction of antioxidants (results obtained in pancreatic cancer cells) | [80, 93] |
Licochalcone A | Induction of apoptosis and prosurvival ULK1/ATG13-mediated autophagy | Activation of autophagic flux | Suppression of the GSH generation and formation of superoxide | [78] |
Bevacizumab | Antiangiogenic effect and induction of prosurvival autophagy | Enhancement of metabolic stress-induced oxidative damage and cytotoxicity | Indirectly obtained by metabolic stress such as starvation and hypoxia | [77] |
OSU-03012 | Autophagic cell death (ACD) | Activation of autophagic flux | Unknown. Mitochondrial superoxide production was demonstrated for the analogue Celecoxib | [83, 94] |
DHEA | ACD | No involvement in autophagic commitment | Decrease of GSH/GSSG ratio and impaired pentose phosphate pathway | [86] |
Tetrandrine | Apoptosis (high concentrations) and ACD (low concentrations) | Activation of ERK-mediated autophagic flux | Mitochondrial dysfunction | [87] |
Adpa-Mn | Apoptosis and ACD | Induction of both apoptosis and autophagy | Mitochondrial dysfunction | [88] |
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