DATS sensitizes glioma cells to TRAIL-mediated apoptosis by up-regulation of death receptor 5 via ROS

Hwang, Jung Soon; Lee, Yong Yook; Lee, Dae-Hee; Kwon, Ki Han

doi:10.1016/j.fct.2017.05.056

Cited by 17 publications

(10 citation statements)

References 29 publications

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“…Our current study confirmed the effects of DATS on attenuation of high glucose-induced HUVEC cytoplasmic and mitochondrial ROS production. However, our current data are not consistent with other studies showing that DATS can induce tumor cell apoptosis and ROS generation in human gastric carcinoma cells [34], glioma cells [35], and osteosarcoma cells [36]. These data speculate that the effects of DATS are cell type dependent, e.g., normal versus tumor cells, thus requiring further investigation.…”

Section: Discussioncontrasting

confidence: 99%

Diallyl trisulfide attenuates hyperglycemia-induced endothelial apoptosis by inhibition of Drp1-mediated mitochondrial fission

et al. 2019

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AimsHyperglycemia induces endothelial cell apoptosis and blood vessel damage, while diallyl trisulfide (DATS) has shown cardiovascular protection in animal models and humans. The aim of this study was to investigate the effects of DATS on inhibition of high glucose-induced endothelial cell apoptosis and the underlying molecular events.MethodsHuman umbilical vein endothelial cells (HUVECs) were incubated with DATS (100 μM) for 30 min and then cultured in high-glucose medium (HG, 33 mM) for 24 h for assessment of apoptosis, glutathione (GSH), reactive oxygen species (ROS), superoxide dismutase (SOD), and gene expression using the terminal deoxyuridine triphosphate nick end labeling (TUNEL), flow cytometry, caspase-3 activity, ROS, SOD, and western blot assays as well as JC-1 and MitoTracker Red staining, respectively.ResultsDATS treatment significantly inhibited high glucose-induced HUVEC apoptosis by blockage of intracellular and mitochondrial ROS generation, maintenance of the mitochondrial membrane potential, and suppression of high glucose-induced dynamin-related protein 1 (Drp1) expression. Furthermore, DATS blockage of high glucose-induced mitochondrial fission and apoptosis was through adenosine monophosphate-activated protein kinase (AMPK) activation-inhibited Drp1 expression in HUVECs.ConclusionsDATS demonstrated the ability to inhibit high glucose-induced HUVEC apoptosis via suppression of Drp1-mediated mitochondrial fission in an AMPK-dependent fashion.

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Section: Discussioncontrasting

confidence: 99%

Diallyl trisulfide attenuates hyperglycemia-induced endothelial apoptosis by inhibition of Drp1-mediated mitochondrial fission

et al. 2019

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“…11,30,38,39 In this study, our results found that ROS generation is critical for CSC-3436-induced upregulation of DR5. Our data regarding CSC-3436-induced upregulation of DR5 through ROS generation were consistent with those in previous reports regarding bufalin, 40 telmisartan, 41 diallyl trisulfide, 42 and plumbagin. 43 We also revealed ROS has been shown to induce MAPK, 11,14,41,44,45 it is possible that CSC-3436 induced DR5 upregulation through the activation of ROS and MAPK.…”

Section: Discussionsupporting

confidence: 92%

CSC‐3436 sensitizes triple negative breast cancer cells to TRAIL‐induced apoptosis through ROS‐mediated p38/CHOP/death receptor 5 signaling pathways

Huang

Lin

Chou

et al. 2021

Environmental Toxicology

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Tumor necrosis factor-related apoptosis-induced ligand (TRAIL) shows little or no toxicity in most normal cells and preferentially induces apoptosis in a variety of malignant cells. However, patients develop resistance to TRAIL, therefore, sensitizing agents that can sensitize the tumor cells to TRAIL-mediated apoptosis are necessary. In this study, we investigated the effect of 2-(3-hydroxyphenyl)-5-methylnaphthyridin-4-one (CSC-3436), an useful flavonoid, to overcome the TRAIL-resistant triple negative breast cancer (TNBC) cells. We found that CSC-3436 potentiated TRAIL-induced apoptosis in TRAIL-resistant TNBC cells and this correlated with the upregulation of death receptors (DR)-5 and down-regulation of decreased decoy receptor (DcR)-1 expression.When examined for its mechanism, we found that the decreased expression of antiapoptotic proteins c-FLIPS/L, Bcl-Xl, Bcl-2, Survivin, and XIAP. CSC-3436 would increase the expression of Bax and promoted the cleavage of bid. In addition, the induction of DR5 by CSC-3436 was found to be dependent on the modulation of reactive oxygen species (ROS)/p38/C/EBP-homologous protein (CHOP) signaling pathways. Overall, our results indicated that CSC-3436 could potentiate the apoptotic

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“…It’s reported that CSFV-induced autophagy limits apoptosis by inhibiting both the intrinsic and extrinsic mechanisms 19 . In addition, ROS is reported to involve in both intrinsic and extrinsic apoptosis 26 , 27 . Therefore, CSFV might also exploit FHC to limits both intrinsic and extrinsic apoptosis, and this point will be further investigated.…”

Section: Discussionmentioning

confidence: 99%

FHC, an NS4B-interacting Protein, Enhances Classical Swine Fever Virus Propagation and Acts Positively in Viral Anti-apoptosis

Gui

Lin

et al. 2018

Sci Rep

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Classical swine fever virus (CSFV), the etiological agent of classical swine fever, causes enormous economic loss to the pig industry. Ferritin heavy chain (FHC) is a notable anti-apoptotic protein, and existing evidence suggests that CSFV cannot induce apoptosis of host cells, however, the role of FHC in CSFV replication remains unclear. In the present study, we found that recombinant lentivirus-mediated knockdown or overexpression of FHC inhibited or enhanced CSFV replication, respectively, indicating a positive role for FHC in CSFV proliferation. Furthermore, interaction between the CSFV NS4B protein and FHC was confirmed by glutathione S-transferase (GST) pull-down, co-immunoprecipitation (co-IP) and confocal imaging assays. In addition, both CSFV replication and NS4B expression upregulated expression of FHC, which counteracts apoptosis by modulating cellular reactive oxygen species (ROS). These results suggest that FHC, an NS4B-interacting protein, enhances CSFV replication and has a positive role in viral anti-apoptosis by regulating ROS accumulation. This work may provide a new perspective for understanding the mechanism of CSFV pathogenesis.

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DATS sensitizes glioma cells to TRAIL-mediated apoptosis by up-regulation of death receptor 5 via ROS

Cited by 17 publications

References 29 publications

Diallyl trisulfide attenuates hyperglycemia-induced endothelial apoptosis by inhibition of Drp1-mediated mitochondrial fission

Diallyl trisulfide attenuates hyperglycemia-induced endothelial apoptosis by inhibition of Drp1-mediated mitochondrial fission

CSC‐3436 sensitizes triple negative breast cancer cells to TRAIL‐induced apoptosis through ROS‐mediated p38/CHOP/death receptor 5 signaling pathways

FHC, an NS4B-interacting Protein, Enhances Classical Swine Fever Virus Propagation and Acts Positively in Viral Anti-apoptosis

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