Viral IL-10 down-regulates the “MHC-I antigen processing operon” through the NF-κB signaling pathway in nasopharyngeal carcinoma cells

Ren, Yanping; Yang, Jie; Sun, Ramon C.; Zhang, Lijuan; Zhao, Liufang; Li, Baozhong; Lei, Li; Long, Haiting; Sun, Qing‐Yuan; Huang, Yunchao; Li, Xiaojiang

doi:10.1007/s10616-016-9987-9

Cited by 13 publications

(7 citation statements)

References 25 publications

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“…28 In the nucleus, NF-κB bonded to gene promoters in their transcriptional regulatory regions, triggering a sequence of physiological or pathological effects such as an inflammatory response. 46,47 Our previous studies have found that the activation of the NF-κB signaling pathway played an important role in pulmonary toxicity induced by nano NiO. 7 Liu et al 38 reported that nickel sulfate could induce oxidative stress and inflammatory responses in mice liver through TLR4/p38/NF-κB, upregulating the TNF-α and NF-κB protein expression levels.…”

Section: Discussionmentioning

confidence: 98%

Nano NiO induced liver toxicity via activating the NF-κB signaling pathway in rats

et al. 2017

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Studies have demonstrated that nano NiO could induce liver toxicity in rats, but its mechanism remains unclear. This study aimed to explore the role of the NF-κB signaling pathway in rat liver toxicity after nano NiO exposure. Male Wistar rats were exposed to nano NiO (0.015, 0.06 and 0.24 mg per kg b.w.) and micro NiO (0.24 mg per kg b.w.) by intratracheal instillation twice a week for 6 weeks. To investigate the liver toxicity induced by nano NiO, the indicators of liver function and inflammatory response were detected, and the histopathological changes were observed. The levels of NF-κB signaling pathway related gene and protein expression were examined using RT-qPCR and western blot techniques in the liver tissue. The results showed that the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and gamma-glutamyltranspeptidase (GGT) increased after nano NiO exposure. Cellular edema, hepatic sinus disappearance, and neutrophil and lymphocyte infiltration were observed. Nano NiO increased the concentrations of pro-inflammatory cytokines (IL-1β and IL-6), but decreased the levels of anti-inflammatory cytokines (IL-4 and IL-10). It also induced the upregulation of TNF-α, NF-κB-inducible kinase (NIK), IκB kinase alpha (IKK-α) and NF-κB mRNA, while inducing the downregulation of the inhibitor kappa B (IκB) alpha. In addition, we found that the protein content of NIK, IKK-α, p-IKK-α, p-IκB-α and NF-κB was elevated, whereas that of IκB-α was reduced. The results indicated that the NF-κB signaling pathway played an important role in rat liver toxicity induced by nano NiO.

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Section: Discussionmentioning

confidence: 98%

Nano NiO induced liver toxicity via activating the NF-κB signaling pathway in rats

et al. 2017

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“…Previous evidence showed that NF-κB, a pivotal transcription factor, is a heterodimer consisting of p50 and RelA/p65 subunits. Dysfunction of NF-κB is involved in various diseases [ 34 ]. In nonstimulated cells, NF-κB p65 locates in the cytoplasm where it is bound to its inhibitor protein IκBα; however, the p65 subunit dissociates from the NF-κB p65 complex and translocates to the nucleus in response to cell insults produced by a high glucose concentration [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Trichosanthes kirilowii lectin alleviates diabetic nephropathy by inhibiting the LOX1/NF-κB/caspase-9 signaling pathway

Peng

Xiang

et al. 2018

Bioscience Reports

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Trichosanthes kirilowii lectin (TKL) has been reported to exert hypoglycemic effects in alloxan-induced diabetic mice. However, there is no evidence showing that it helps to prevent diabetic nephropathy (DN). We used a high glucose (HG)-induced HK-2 cell model and a streptozocin (STZ)-induced Wistar rat model to investigate the effects of TKL on DN, as well as the mechanisms for those effects. Our results showed that TKL significantly increased the viability of HG-treated HK-2 cells and inhibited cell apoptosis. In vivo experiments demonstrated that TKL attenuated STZ-induced histopathological damage and the inflammatory response in rat kidney tissues. Pre-treatment of HK-2 cells or STZ-treated rats with polyinosinic acid (Poly IC), an inhibitor of lectin-like oxLDL receptor 1 (LOX1), blocked the protective effect of TKL against HG- or STZ-induced damage to kidney tissue, indicating that TKL might exert its effect via LOX1-mediated endocytosis. Additional results suggested that TKL inhibits the phosphorylation of IκB kinase β (IKKβ) and the nuclear factor-κB (NF-κB) inhibitor protein (IκBα), and thereby reduces the nuclear translocation of NF-κB (p65). ChIP assay data indicated that TKL markedly inhibits the binding of p65 to the CASP9 gene in HG-treated HK-2 cells, subsequently suppressing transcription of the CASP9 gene. In the dual-luciferase reporter assay, TKL significantly inhibited luciferase activity in cells co-transfected with p65 and a wild-type capase-9 construct instead of mutated caspase-9 constructs.Taken together, our results show that TKL helps to protect against DN by inhibiting the LOX1/NF-κB/caspase-9 signaling pathway, suggesting TKL as a promising agent for treating DN.

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“…The immortalized EVB negative NPC cell lines, CNE1 and CNE2, were kept from the previous research 21. The EVB positive NPC cell line, C666‐1, was obtained from the Cancer Research Institute of Southern Medical University.…”

Section: Methodsmentioning

confidence: 99%

“…The total proteins from different treatments were extracted according to the previously published paper 21. The expression levels of targeted proteins were then measured by Western blot (WB) assay.…”

Section: Methodsmentioning

confidence: 99%

“…Naive human B cells could be stimulated by hIL‐10 and then secret immunoglobulin A by cooperating with transforming growth factor β to activate the generation of anti‐CD40 cell 12. Comparison with hIL‐10, vIL‐10 has the similar immunosuppressive effects of hIL‐10 but without the immunostimulatory effects of hIL‐10 including the augmentation of CTL proliferation and the expansion of B cell 13,14. But by now, the function of vIL‐10 in the cancer cell proliferation has not been well illustrated.…”

Section: Introductionmentioning

confidence: 99%

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Viral IL‐10 promotes cell proliferation and cell cycle progression via JAK2/STAT3 signaling pathway in nasopharyngeal carcinoma cells

Ren

Yang

et al. 2020

Biotech and App Biochem

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Epstein–Barr virus (EBV) is positively related to the morbidity of nasopharyngeal carcinoma (NPC) in Asia. After infection, EBV can produce several proteins, including viral interleukin‐10 (vIL‐10). But the mechanism by which vIL‐10 contributes to NPC cell proliferation and cell cycle progression is not well understood. In this study, EBV negative and positive cell lines, and the JAK2/STAT3 signal pathway inhibitor AG490 were used to illustrate the role of vIL‐10 in NPC. Cell proliferation and cell cycle were measured by CCK‐8 and flow cytometry. The expression levels of related protein were measured by Western blotting. High concentrations of vIL‐10 and IL‐6 were found in the EBV positive patients. The expression level of IL‐6 was positively related to the presence of concentration of vIL‐10. vIL‐10 can promote cancer cell proliferation and G1 to S phase transmission via upregulating the IL‐6 protein level by activating the JAK2/STAT3 signal pathway. Furthermore, EBV can induce the formation of cytotoxic T cells, whereas vIL‐10 can block the function of cytotoxic T cells. Taken together, these results suggest that vIL‐10 promotes cell proliferation and cell cycle progression via JAK2/STAT3 signaling pathway in NPC.

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Viral IL-10 down-regulates the “MHC-I antigen processing operon” through the NF-κB signaling pathway in nasopharyngeal carcinoma cells

Abstract: The HLA-I antigen processing machinery (APM) plays a crucial role in the anticancer immune response. The loss of surface expression of HLA

Cited by 13 publications

References 25 publications

Nano NiO induced liver toxicity via activating the NF-κB signaling pathway in rats

Nano NiO induced liver toxicity via activating the NF-κB signaling pathway in rats

Trichosanthes kirilowii lectin alleviates diabetic nephropathy by inhibiting the LOX1/NF-κB/caspase-9 signaling pathway

Viral IL‐10 promotes cell proliferation and cell cycle progression via JAK2/STAT3 signaling pathway in nasopharyngeal carcinoma cells

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