Autocrine TNF-α-mediated NF-κB activation is a determinant for evasion of CD40-induced cytotoxicity in cancer cells

Li, Daoxia; Zhong, Yang; Zhou, Yuqiong; Sun, Hong; Zheng, Xuelian; Zhao, Chen; Yan, Youyi; Lin, Yong; Liao, Linchuan; Wang, Xia

doi:10.1016/j.bbrc.2013.05.128

Cited by 9 publications

(10 citation statements)

References 20 publications

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“…NF-κB is a major transcription factor that regulates various cell processes, such as embryonic development, immunity, apoptosis, angiogenesis and proliferation [19]. The NF-κB family is composed of five members (RelA or p65, RelB, c-Rel, p50 and p52).…”

Section: Discussionmentioning

confidence: 99%

Dihydroartemisinin Accentuates the Anti-Tumor Effects of Photodynamic Therapy via Inactivation of NF-κB in Eca109 and Ec9706 Esophageal Cancer Cells

Zhou

et al. 2014

Cell Physiol Biochem

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Background: Photodynamic therapy (PDT) is a new treatment for esophageal cancer which has been shown to be effective in the elimination of tumor. However, PDT could induce the activation of nuclear factor-kappa B (NF-κB) in many photosensitizers based PDT, which plays a negative role in PDT. In addition, our previous results have shown that dihydroartemisinin (DHA), which was the most potent one of artemisinin derivatives, has anticancer activity in esophageal cancer cells. Methods: Cell viability was determined by MTT analysis, and apoptosis was evaluated by flow cytometry. Nuclear extract was obtained for determining NF-κB DNA-binding activity, while total protein extract obtained for downstream gene expression by western blot. Results: We demonstrated DHA enhanced PDT-induced growth inhibition and apoptosis in both human esophageal cancer cell lines Eca109 and Ec9706 in vitro. The mechanism was at least partially due to DHA deactivated PDT-induced NF-κB activation, so as to decrease tremendously the expression of its target gene Bcl-2. Conclusion: Our results demonstrate that DHA augments PDT-induced growth inhibition and apoptosis in esophageal cancer cells, and that inactivation of NF-κB activity is a potential mechanism by which DHA sensitizes esophageal cancer cells to PDT-induced growth inhibition and apoptosis.

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Section: Discussionmentioning

confidence: 99%

Dihydroartemisinin Accentuates the Anti-Tumor Effects of Photodynamic Therapy via Inactivation of NF-κB in Eca109 and Ec9706 Esophageal Cancer Cells

Zhou

et al. 2014

Cell Physiol Biochem

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“…Elevated levels of inflammation-related molecules within PDT-targeted tissue, such as NF-κB and cyclooxygenase-2 (COX-2), could reduce the antitumor effectiveness of PDT by facilitating survival of residual tumor cells, [ 18 , 19 , 20 , 21 , 22 ]. NF-κB is a major transcription factor that regulates various cell processes, such as apoptosis, inflammation, proliferation, angiogenesis and immunity [ 23 ]. COX-2 is overexpressed in many types of cancer and is considered to be associated with reduced patient survival [ 24 ].…”

Section: Introductionmentioning

confidence: 99%

Brazilian Green Propolis Extract Synergizes with Protoporphyrin IX-mediated Photodynamic Therapy via Enhancement of Intracellular Accumulation of Protoporphyrin IX and Attenuation of NF-κB and COX-2

Wang

et al. 2017

Molecules

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Brazilian green propolis (BGP) is noted for its impressive antitumor effects and has been used as a folk medicine in various cultures for many years. It has been demonstrated that BGP could enhance the cytotoxic effect of cytostatic drugs on tumor cells. Photodynamic therapy (PDT) is a therapeutic approach used against malignant cells. To assess the synergistic effect of BGP extract on protoporphyrin IX (PpIX)-mediated photocytotoxicity, MTT assays were performed using A431 and HeLa cells. TUNEL assay and Annexin V-FITC/PI staining were performed to confirm the induction of apoptosis. Western blotting analysis was performed to examine the pro-apoptotic proteins, anti-apoptotic proteins and inflammation related proteins in A431 cells. Intracellular accumulation of PpIX was examined by flow cytometry. The synergistic effect of BGP extract in PpIX-PDT was also evaluated with a xenograft model. Our findings reveal that BGP extract increased PpIX-mediated photocytotoxicity in A431 and HeLa cells. PpIX-PDT with BGP extract treatment resulted in a decrease in Bcl-xL and an increase in NOXA, Bax and caspase-3 cleavage. The protein expression levels of p-IKKα/β, NF-κB and COX-2 were upregulated by PpIX-PDT but significantly attenuated when in combination with BGP extract. BGP extract was also found to significantly enhance the intracellular accumulation of PpIX in A431 cells. BGP extract increased PpIX-mediated photocytotoxicity in a xenograft model as well. Our findings provide evidence for a synergistic effect of BGP extract in PpIX-PDT both in vitro and in vivo.

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“…11 The primary role of TNF-α is in the regulation of immune cells, and is able to induce apoptosis. 12 …”

Section: Introductionmentioning

confidence: 99%

Simvastatin Reduces Burn Injury-induced Splenic Apoptosis via Downregulation of the TNF-α/NF-κB Pathway

Zhao

Kaneki

et al. 2015

Annals of Surgery

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Objective Recent studies have suggested that epidermal burn injuries are associated with inflammation and immune dysfunction. Simvastatin has been shown to possess potent anti-inflammatory properties. Thus we hypothesized that simvastatin protects against burn-induced apoptosis in spleen via its anti-inflammatory activity. Methods Wild-type, tumor necrosis factor alpha knockout (TNF-αKO) and NF-κB KO mice were subjected to full-thickness burn injury or sham treatment. The mice then were treated with or without simvastatin and the spleen were harvested to measure the extent of apoptosis. Expression levels of TNF-αand NF-κB were also determined in spleen tissue and serum. Results Burn injury induced significant splenic apoptosis and systemic cytokine production. Simvastatin protected the spleen from apoptosis, reduced cytokine production in the serum and increased the survival rate. Simvastatin decreased burn-induced TNF-αand NF-κB expression in spleen and serum. TNF-αand NF-κB KO mice demonstrated lower levels of apoptosis in spleen in response to burn. Simvastatin did not further decrease burn-caused apoptosis and mortality in either strain of KO mice. Conclusions Simvastatin reduces burn-induced splenic apoptosis via down-regulation of the TNF-α/ NF-κB pathway.

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Autocrine TNF-α-mediated NF-κB activation is a determinant for evasion of CD40-induced cytotoxicity in cancer cells

Cited by 9 publications

References 20 publications

Dihydroartemisinin Accentuates the Anti-Tumor Effects of Photodynamic Therapy via Inactivation of NF-κB in Eca109 and Ec9706 Esophageal Cancer Cells

Dihydroartemisinin Accentuates the Anti-Tumor Effects of Photodynamic Therapy via Inactivation of NF-κB in Eca109 and Ec9706 Esophageal Cancer Cells

Brazilian Green Propolis Extract Synergizes with Protoporphyrin IX-mediated Photodynamic Therapy via Enhancement of Intracellular Accumulation of Protoporphyrin IX and Attenuation of NF-κB and COX-2

Simvastatin Reduces Burn Injury-induced Splenic Apoptosis via Downregulation of the TNF-α/NF-κB Pathway

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Autocrine TNF-α-mediated NF-κB activation is a determinant for evasion of CD40-induced cytotoxicity in cancer cells

Cited by 9 publications

References 20 publications

Dihydroartemisinin Accentuates the Anti-Tumor Effects of Photodynamic Therapy via Inactivation of NF-&#954;B in Eca109 and Ec9706 Esophageal Cancer Cells

Dihydroartemisinin Accentuates the Anti-Tumor Effects of Photodynamic Therapy via Inactivation of NF-&#954;B in Eca109 and Ec9706 Esophageal Cancer Cells

Brazilian Green Propolis Extract Synergizes with Protoporphyrin IX-mediated Photodynamic Therapy via Enhancement of Intracellular Accumulation of Protoporphyrin IX and Attenuation of NF-κB and COX-2

Simvastatin Reduces Burn Injury-induced Splenic Apoptosis via Downregulation of the TNF-α/NF-κB Pathway

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Dihydroartemisinin Accentuates the Anti-Tumor Effects of Photodynamic Therapy via Inactivation of NF-κB in Eca109 and Ec9706 Esophageal Cancer Cells

Dihydroartemisinin Accentuates the Anti-Tumor Effects of Photodynamic Therapy via Inactivation of NF-κB in Eca109 and Ec9706 Esophageal Cancer Cells