Reactive oxygen species regulate caspase activation in tumor necrosis factor-related apoptosis-inducing ligand-resistant human colon carcinoma cell lines.

@article{Izeradjene2005ReactiveOS,
  title={Reactive oxygen species regulate caspase activation in tumor necrosis factor-related apoptosis-inducing ligand-resistant human colon carcinoma cell lines.},
  author={Kamel Izeradjene and Leslie Douglas and David M. Tillman and Addison B Delaney and Janet A. Houghton},
  journal={Cancer research},
  year={2005},
  volume={65 16},
  pages={
          7436-45
        }
}
The effects of reactive oxygen species (ROS) on tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in solid cancers have yet to be clearly defined. In this study, we found that the classic uncoupler of oxidative phosphorylation, carbonyl cyanide m-chlorophenylhydrazone (CCCP), induced a reduction in DeltaPsim and generation of ROS. This uncoupling effect enhanced TRAIL-induced apoptosis in TRAIL-resistant human colon carcinoma cell lines (RKO, HT29, and HCT8… 
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Reactive Oxygen Species Mediate Caspase Activation and Apoptosis Induced by Lipoic Acid in Human Lung Epithelial Cancer Cells through Bcl-2 Down-Regulation
TLDR
A novel pro-oxidant role of LA is indicated in apoptosis induction and its regulation by Bcl-2, which may be exploited for the treatment of cancer and related apoptosis disorders.
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The mechanistic data indicate that sorafenib bypasses central resistance mechanisms through a direct induction of ΔΨm breakdown and ROS production and leads to apoptosis that involves activation of an amplification loop via the mitochondrial apoptosis pathway.
Reactive Oxygen Species Mediate Caspase Activation and Apoptosis Induced by Lipoic Acid in Human Lung Epithelial Cancer Cells through Bcl-2 Downregulation
TLDR
It is reported here that LA induced reactive oxygen species (ROS) generation and a concomitant increase in apoptosis of human lung epithelial cancer H460 cells, indicating a novel pro-oxidant role of LA in apoptotic induction and its regulation by Bcl-2, which may be exploited for the treatment of cancer and related apoptosis disorders.
Reactive oxygen species regulate Bax translocation and mitochondrial transmembrane potential, a possible mechanism for enhanced TRAIL-induced apoptosis by CCCP.
TLDR
The results suggest that uncoupling the cells by CCCP can overcome the resistance to TRAil protein and can be a very efficient treatment for the tumor cells especially resistant to TRAIL-induced apoptosis.
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TLDR
TRAIL is a member of the tumor necrosis factor family and engages apoptosis via recruitment and rapid activation of caspase-8, suggesting that treatment with CCCP combined with that with TRAIL can be an efficient method to induce death of tumor cells, particularly cells that are resistant to TRAIL-induced apoptosis.
The essential role of the mitochondria and reactive oxygen species in Cisplatin-mediated enhancement of fas ligand-induced apoptosis in malignant pleural mesothelioma.
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TLDR
In follicular undifferentiated thyroid cells, S-nitrosylation and nuclear translocation of GAPDH appear to mediate TRAIL-induced cell death at least partially, as evidenced by pretreatment with N- Nitro-L-arginine methyl ester, a competitive nitric oxide synthase inhibitor that partially but significantly attenuated TRAil-induced apoptosis.
Mitochondrial superoxide mediates mitochondrial and endoplasmic reticulum dysfunctions in TRAIL-induced apoptosis in Jurkat cells.
Cisplatin enhances the antitumor effect of tumor necrosis factor-related apoptosis-inducing ligand gene therapy via recruitment of the mitochondria-dependent death signaling pathway
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This study evaluated the ability of cisplatin to enhance the cytotoxic effect of TRAIL gene therapy using the recombinant adenovirus-mediated tumor-selective expression of membrane-bound green fluorescence protein (GFP)-TRAIL fusion protein on thoracic cancer cells and elucidate the putative mechanisms responsible for this synergistic combination effect.
CCT 327 enhances TRAIL-induced apoptosis through the induction of death receptors and downregulation of cell survival proteins in TRAIL-resistant human leukemia cells
TLDR
Results showed that CCT327 combined with TRAIL treatment may provide an effective therapeutic strategy for cancer.
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