Transcriptional Regulation of Cyclooxygenase-2 in Response to Proteasome Inhibitors Involves Reactive Oxygen Species-mediated Signaling Pathway and Recruitment of CCAAT/Enhancer-binding Protein δ and CREB-binding Protein

Chen, Jun Jie; Huang, Wei; Chen, Ching-Chow

doi:10.1091/mbc.e05-08-0778

Cited by 81 publications

(58 citation statements)

References 50 publications

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“…Cells were then rapidly washed with PBS and lysed with ice-cold lysis buffer (50 mM Tris-HCl (pH 7.4), 1 mM EGTA, 1 mM NaF, 150 mM NaCl, 1 mM PMSF, 5 g/ml leupeptin, 20 g/ml aprotinin, 1 mM Na 3 VO 4 , 10 mM ␤-glycerophosphate, 5 mM Na 4 P 2 O 7 , and 1% Triton X-100), as previously described (16).…”

Section: Preparation Of Total Cell Lysates and Nuclear Extractsmentioning

confidence: 99%

“…Binding of transcription factors to the DR5 intron was assayed as previously described (16). The nuclear extract (400 g) was precleared at room temperature for 1 h with 20 l of the 4% streptavidin-coated beads (SigmaAldrich) mixed with 50% slurry to reduce nonspecific binding.…”

Section: Dna Affinity Protein-binding Assay (Dapa)mentioning

confidence: 99%

“…ChIP assay analysis was performed as previously described (16). DNA immunoprecipitated by p53 and p65 Abs was purified.…”

Section: Chip Assaymentioning

confidence: 99%

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Proteasome Inhibitors Enhance TRAIL-Induced Apoptosis through the Intronic Regulation of DR5: Involvement of NF-κB and Reactive Oxygen Species-Mediated p53 Activation

Chen

Chou

Chang

et al. 2008

The Journal of Immunology

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Manipulation of TRAIL receptor 2 (DR5) pathway is a promising therapeutic strategy to overcome TRAIL-resistant lung cancer cells. Preclinical studies have shown that proteasome inhibitors enhance TRAIL-induced apoptosis in lung cancer cells, but the underlying mechanism has not been fully elucidated. In this study, we demonstrated the enhancement of TRAIL-mediated apoptosis in human alveolar epithelial cells by proteasome inhibitors that up-regulate DR5 expression. This effect was blocked by DR5-neutralizing Ab. Using reporter assay, we demonstrated that the p53 and NF-κB elements on the DR5 first intron region were involved in proteasome inhibitor-induced DR5 expression. Both p53 small interfering RNA and NF-κB inhibitor suppressed DR5 expression, strengthening the significance of p53 and NF-κB in DR5 transcription. The protein stability, Ser392 phosphorylation and Lys373/Lys382 acetylation of p53 were enhanced by MG132. In addition to p53, IκBα degradation and NF-κB translocation was also observed. Moreover, the binding of p53 and p65 to the first intron of DR5 was demonstrated by DNA affinity protein-binding and chromatin immunoprecipitation assays. Intracellular reactive oxygen species (ROS) generation after MG132 treatment contributed to p53, but not p65 nuclear translocation and DNA-binding activity. ROS scavenger dramatically inhibited the apoptosis induced by proteasome inhibitors plus TRAIL. The p53-null H1299 cells were resistant to proteasome inhibitor-induced DR5 up-regulation and enhancement of TRAIL-induced apoptosis. These findings reveal that proteasome inhibitor-mediated NF-κB and ROS-dependent p53 activation are contributed to intronic regulation of DR5 transcription, and resulted in the subsequent enhancement of TRAIL-induced apoptosis in human lung cancer cells.

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Section: Preparation Of Total Cell Lysates and Nuclear Extractsmentioning

confidence: 99%

Section: Dna Affinity Protein-binding Assay (Dapa)mentioning

confidence: 99%

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Proteasome Inhibitors Enhance TRAIL-Induced Apoptosis through the Intronic Regulation of DR5: Involvement of NF-κB and Reactive Oxygen Species-Mediated p53 Activation

Chen

Chou

Chang

et al. 2008

The Journal of Immunology

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“…Previous studies have demonstrated that, during inflammation, C/EBPδ is recruited to the promoter region of cyclooxygenase-2, although its expression levels remained constant (19). Currently, to the best of our knowledge, no conclusive study of the expression levels of C/EBPδ in GC cells has been performed.…”

Section: Discussionmentioning

confidence: 95%

CCAAT/enhancer-binding protein α decreases the viability of gastric cancer cells

Tomizawa¹,

Shinozaki²,

Motoyoshi³

et al. 2017

Oncology Letters

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Abstract. CCAAT/enhancer-binding protein (C/EBP) α, C/EBPβ and C/EBPδ are involved in inflammation and cell differentiation. In the present study, their roles in human gastric cancer cells were investigated. The human gastric cancer cell lines MKN45 and MKN74 were subjected to the reverse transcription-quantitative polymerase chain reaction (RT-qPCR) to analyze the expression levels of C/EBPα, C/EBPβ and C/EBPδ. The cells were transfected with expression plasmids for either C/EBPα or C/EBPδ, and subjected to a 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium inner salt (MTS) assay and RT-qPCR for analysis of cyclin D1 expression. Expression levels of C/EBPα and C/EBPδ were decreased in MKN45 and MKN74 cells compared with in normal gastric tissue. Expression levels of C/EBPβ were decreased in MKN45 cells and increased in MKN74 cells. Viability of MKN45 cells was decreased by C/EBPα and C/EBPδ. Viability of MKN74 cells was decreased by C/EBPα, but increased by C/EBPδ. Expression levels of cyclin D1 were decreased in association with C/EBPα and C/EBPδ overexpression in MKN45 cells. Expression levels of cyclin D1 were decreased in association with C/EBPα overexpression, but increased in association with C/EBPδ overexpression, in MKN74 cells. The results of the present study indicate that C/EBPα is potentially useful for the treatment of gastric cancer.

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“…NF-κB is a vital regulator of a number of proinflammatory genes, including iNOS, COX-2, TNF-α, IL-1β, and IL-6, in LPS-induced inflammation. [21][22][23] Generally, the inactive complex of NF-κB with IκB exists in the cytoplasm. IκB is rapidly phosphorylated in response to proinflammatory stimuli, leading to dissociation of the complex.…”

mentioning

confidence: 99%

Luteolin 5-O-glucoside from Korean Milk Thistle,Cirsium maackii, Exhibits Anti-Inflammatory Activity via Activation of the Nrf2/HO-1 Pathway

et al. 2017

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-Luteolin 5-O-glucoside is the major flavonoid from Korean thistle, Cirsium maackii. We previously reported the anti-inflammatory activities of luteolin 5-O-glucoside in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. In this study, we determined the anti-inflammatory mechanisms of luteolin 5-O-glucoside through the inhibition of nitric oxide (NO) production in vitro and in vivo. Results revealed that luteolin 5-O-glucoside dosedependently inhibited NO production and expression of iNOS and COX-2 in LPS-induced RAW 264.7 cells. Luteolin 5-O-glucoside also significantly inhibited the translocation of NF-κB, the activation of MAPKs, and ROS generation in LPS-induced RAW 264.7 cells. In addition, protein expressions of Nrf-2 and HO-1 were also upregulated by luteolin 5-O-glucoside treatment. Moreover, luteolin 5-O-glucoside inhibited λ-carrageenaninduced mouse paw edema by 65.34% and 48.31% at doses of 50 and 100 mg/kg body weight, respectively. These findings indicate potential anti-inflammatory effect of luteolin 5-O-glucoside particularly by downregulating NF-κB and upregulating HO-1/Nrf-2 pathway.

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Transcriptional Regulation of Cyclooxygenase-2 in Response to Proteasome Inhibitors Involves Reactive Oxygen Species-mediated Signaling Pathway and Recruitment of CCAAT/Enhancer-binding Protein δ and CREB-binding Protein

Cited by 81 publications

References 50 publications

Proteasome Inhibitors Enhance TRAIL-Induced Apoptosis through the Intronic Regulation of DR5: Involvement of NF-κB and Reactive Oxygen Species-Mediated p53 Activation

Proteasome Inhibitors Enhance TRAIL-Induced Apoptosis through the Intronic Regulation of DR5: Involvement of NF-κB and Reactive Oxygen Species-Mediated p53 Activation

CCAAT/enhancer-binding protein α decreases the viability of gastric cancer cells

Luteolin 5-O-glucoside from Korean Milk Thistle,Cirsium maackii, Exhibits Anti-Inflammatory Activity via Activation of the Nrf2/HO-1 Pathway

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