|
Drugs or treatment | Mechanisms | Reference |
|
Gemcitabine | Increasing ROS activated MST1 translocated to mitochondria and formed a complex with the local protein Cyp-D induced death of pancreatic cancer cells | [76] |
|
Eriocalyxin B | Increase the intracellular ROS levels and regulating the MAPK, NF-κB pathways | [77] |
|
Compound 3b | Increase ROS by AKT activation promoted activation of stress kinases (p38/JNK) resulting in pancreatic cancer cell death | [68] |
|
Artemisinin | Induce apoptosis via the generation of ROS and triggering binding of CD95L to CD95 receptor | [78] |
|
Genipin | UCP2 inhibition triggers ROS-dependent nuclear translocation of the glycolytic enzyme glyceraldehyde 3-phosphate dehydrogenase (GAPDH), formation of autophagosomes, and the expression of the autophagy marker LC3-II | [74] |
|
P-V; MDC-1112 | Reduce STAT3 levels in the mitochondria by preventing its translocation from the cytosol and enhanced the mitochondrial levels of ROS which triggered apoptosis | [73] |
|
Noninvasive radiofrequency treatment | Impair the function of mitochondria in cancer cells and increased ROS production | [79] |
|
Green 1 | Increase ROS production in mitochondria | [80] |
|
SKLB316 | Decrease the mitochondrial membrane potential and induce the generation of ROS in cells | [81] |
|
Gemcitabine | Enhance selectively the expression of CXCL8 through ROS generation and NF-κB activation | [82] |
|
Withaferin A combined with oxaliplatin | Enhance mitochondrial dysfunction, inactivation of the PI3K/AKT pathway, and accumulation of intracellular ROS | [69] |
|
Spiclomazine | Reduce the mitochondria membrane potential, elevated ROS, and activated caspase-3/caspase-9 | [71] |
|
Cerium oxide nanoparticles | Sensitization of pancreatic cancer cells to radiation by ROS production | [83] |
|
Oleanolic acid | Arrests the cell cycle and induces apoptosis, possibly via ROS-mediated mitochondrial and lysosomal pathway | [84] |
|
CDDO-Me | Enhance the production of ROS and inhibited the telomerase activity loss of mitochondrial membrane potential and release of cytochrome c from mitochondria ROS-dependent downregulated p-Akt, p-mTOR, and NF-κB (p65) | [85, 86] |
|
Belinostat | Increase ROS-induced transforming growth factor-beta-activating kinase 1 (TAK1)/AMPK association to activate AMPK | [87] |
|
TBMMP | Increase cytochrome c release, reduced mitochondrial membrane potential, activated caspase-3, caspase-9, elevated ROS, and increased expression of Bax | [88] |
|
Isoalantolactone | Induce ROS-dependent apoptosis through intrinsic pathway | [89] |
|
Gallic acid | Activated caspase-3, caspase-9, and reactive oxygen species | [90] |
|
Dihydroartemisinin | DHA enhances Apo2L/TRAIL-mediated apoptosis in human pancreatic cancer cells through ROS-mediated upregulation of death receptor 5 (DR5) | [33] |
|
BML-275 | Induce ROS generation, DNA damage, and apoptosis via inhibition of the AMPK pathway and by inducing G2/M arrest via a pathway independent of AMPK | [91] |
|
Nickel nanowires | Induce ROS-mediated apoptosis | [92] |
|
Fenretinide | Induce apoptosis and autophagy and that sensitivity appears to be mediated by enhanced ROS | [93] |
|
Sulforaphane | Induce autophagy depending on ROS | [94] |
|
Brucein D | Activate redox-sensitive p38-MAPK pathway and inhibition of NF-κB antiapoptotic activity mediated by enhanced ROS | [1] |
|
Artesunate | Induce ROS-mediated apoptosis | [95] |
|
Nitric oxide-donating aspirin | ROS → MAPKs → p21 (cip-1) → cyclin D1 → cell death | [96] |
|
Benzyl isothiocyanate | Activate ERK, JNK, and P38 at leading to the induction of apoptosis mediated by enhanced ROS | [97] |
|
Arsenic trioxide and parthenolide | Induce reactive oxygen species generation and apoptosis via the mitochondrial pathway | [98] |
|
Triphala | Phosphorylation of p53 and ERK induces apoptosis mediated by enhanced ROS | [99] |
|
Capsaicin | Induce apoptosis through ROS generation and mitochondrial death pathway | [100] |
|
Resveratrol | Damage mitochondrial function that leads to increased ROS, apoptosis | [101] |
|