N-Myc-Interacting Protein Negatively Regulates TNF-α-Induced NF-κB Transcriptional Activity by Sequestering NF-κB/p65 in the Cytoplasm

Hou, Jingjing; Jiang, Shihao; Zhao, Jiabao; Zhu, Dong; Zhao, Xinmeng; Cai, Jun; Zhang, Si Qing

doi:10.1038/s41598-017-15074-5

Cited by 17 publications

(8 citation statements)

References 51 publications

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“…Furthermore, intracellular NMI inhibits immune response to reduce inflammatory cytokines in cancer. 25 Therefore, our observation showed that NMI in PBMCs from HBV-ACLF was increased, suggesting that NMI could also serve as an intracellular immune regulator in the development of HBV-ACLF in addition to act as a circulating inflammatory mediator. We acknowledge that there is certain discrepancy of NMI between serum and PBMCs from HCs and CHB.…”

Section: Discussionmentioning

confidence: 60%

“…Our study also showed that NMI was significantly increased in PBMCs from HBV‐ACLF patients, suggesting that upregulated NMI in PBMCs may be related to excessive inflammation response in the development of HBV‐ACLF. Furthermore, intracellular NMI inhibits immune response to reduce inflammatory cytokines in cancer . Therefore, our observation showed that NMI in PBMCs from HBV‐ACLF was increased, suggesting that NMI could also serve as an intracellular immune regulator in the development of HBV‐ACLF in addition to act as a circulating inflammatory mediator.…”

Section: Discussionmentioning

confidence: 69%

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N‐myc and STAT interactor correlates with severity and prognosis in acute‐on‐chronic liver failure of hepatitis B virus

Xiong

Zhou

et al. 2019

J of Gastro and Hepatol

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Background and Aim Hepatitis B virus‐related acute‐on‐chronic liver failure (HBV‐ACLF) is characterized by acute deterioration of chronic liver disease with excessive inflammation. N‐myc and STAT interactor (NMI), an inflammation‐mediated protein, involves in various inflammatory‐related diseases, but the role of NMI in development and prognosis in HBV‐ACLF remains to be elucidated. Methods Serum NMI from healthy controls (HCs, n = 20), chronic hepatitis B (CHB, n = 50) patients, and HBV‐ACLF patients (n = 50) was determined using ELISA. NMI from peripheral blood mononuclear cells and liver was confirmed using quantitative real‐time polymerase chain reaction, Western blot, and immunofluorescence. Results Serum NMI was increased 1.9‐fold or 2.2‐fold from HBV‐ACLF patients compared with that from HCs (P < 0.01) or CHB patients (P < 0.01). Consistently, NMI from peripheral blood mononuclear cells was upregulated significantly from HBV‐ACLF patients compared with that from HCs and CHB patients at mRNA and protein levels. Hepatic NMI from HBV‐ACLF patients was 2.8‐fold higher than that from HCs. Serum NMI was correlated with Model for End‐stage Liver Disease, Chronic Liver Failure Consortium ACLF score, and ACLF grades. In contrast, serum NMI was significantly decreased in HBV‐ACLF ameliorated patients during follow‐up, whereas serum NMI was sustained at high levels in non‐ameliorated patients. Elevated serum NMI (≥ 198.5 pg/mL) was correlated with poor survival rate of HBV‐ACLF patients. Using receiver operating characteristics curves, it was suggested that serum NMI was a potential biomarker in predicting 3‐month mortality of HBV‐ACLF patients. Conclusions Our study highlights the potential role of NMI in assessing the development and prognosis of HBV‐ACLF.

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Section: Discussionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 69%

N‐myc and STAT interactor correlates with severity and prognosis in acute‐on‐chronic liver failure of hepatitis B virus

Xiong

Zhou

et al. 2019

J of Gastro and Hepatol

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“…The NF-κB signaling pathway is closely related to cell proliferation and oncogenesis. In response to numerous stimuli including tumor necrosis factor alpha (TNF-α) and bacterial lipopolysaccharide (LPS), NF-κB is activated and translocated into the nucleus from the cytoplasm, where it acts as a transcription factor to regulate its downstream target genes [35,36,[41][42][43]. In our study, miR-139-5p and PMP22 knockdown both suppress the NF-κB signaling pathway, and PMP22 overexpression rescued the miR-139-5p-induced NF-κB reporter activity, suggesting that PMP22 may enhance tumor proliferation through the NF-κB signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

“…The NF-κB pathway promotes cell proliferation and oncogenesis by protecting cells from apoptosis [35,36]. We speculated that miR-139-5p might regulate PMP22 through the NF-κB pathway.…”

Section: Mir-139-5p Represses Pmp22 By Inhibiting the Nf-κb Pathwaymentioning

confidence: 99%

MiR-139-5p negatively regulates PMP22 to repress cell proliferation by targeting the NF-κB signaling pathway in gastric cancer

et al. 2020

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Gastric cancer (GC) is one of the most common malignant tumors worldwide. Peripheral myelin protein 22 (PMP22) is a 22-kDa tetraspan glycoprotein that is predominantly expressed by myelinating Schwann cells. However, recent studies have shown that PMP22 is closely related to cell proliferation and tumorigenesis in different cancers. In this study, we discovered a new miRNA that regulates PMP22 and gastric cancer cell prolifration. Our bioinformatics analysis suggested that there is a conserved miRNA recognition site for miR-139-5p on the 3' UTR of PMP22. Interestingly, our results showed overexpression of miR-139-5p significantly suppressed growth and prolifration in GC cells and inhibited tumor growth in nude mice xenografted with GC cells. MiR-139-5p suppressed the activity of a luciferase reporter containing the PMP22-3' UTR, and the ectopic expression of PMP22 rescued the miR-139-5p-mediated inhibition of cell proliferation in GC cells. Mechanistically, miR-139-5p may negatively regulate PMP22 to repress cell proliferation by targeting the NF-κB signaling pathway in gastric cancer. Finally, overexpression of miR-139-5p significantly inhibited tumor growth in nude mice xenografted with GC cells.and the miR-139-5p levels were inversely correlated with PMP22 expression in nude mice tumor. Taken together, our data suggest an important regulatory role of miR-139-5p in gastric cancer, suggesting that miR-139-5p and PMP22 might be important diagnostic or therapeutic targets for gastric cancer and other human diseases.

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“…And then, NF-κB is transferred to the nucleus to promote NF-κB-dependent gene transcription. NF-κB mainly regulates the transcriptional effects of IL-6, IL-1β, VCAM-1, COX-2, TNF-α, and JUN [64][65][66][67], thereby mediating the expression of proinflammatory factors to enhance inflammation.…”

Section: Functional Analysis and Pathways Of T2dmmentioning

confidence: 99%

Integrated Analysis of the Mechanisms of Da‐Chai‐Hu Decoction in Type 2 Diabetes Mellitus by a Network Pharmacology Approach

Ren

Tan

Xiong

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Background. The incidence of type 2 diabetes mellitus (T2DM) has increased year by year, which not only seriously affects people’s quality of life, but also imposes a heavy economic burden on the family, society, and country. Currently, the pathogenesis, diagnosis, and treatment of T2DM are still unclear. Therefore, exploration of a precise multitarget treatment strategy is urgent. Here, we attempt to screen out the active components, effective targets, and functional pathways of therapeutic drugs through network pharmacology with taking advantages of traditional Chinese medicine (TCM) formulas for multitarget holistic treatment of diseases to clarify the potential therapeutic mechanism of TCM formulas and provide a systematic and clear thought for T2DM treatment. Methods. First, we screened the active components of Da-Chai-Hu Decoction (DCHD) by absorption, distribution, metabolism, excretion, and toxicity (ADME/T) calculation. Second, we predicted and screened the active components of DCHD and its therapeutic targets for T2DM relying on the Traditional Chinese Medicine Systems Pharmacology Analysis Platform (TCMSP database) and Text Mining Tool (GoPubMed database), while using the Database for Annotation, Visualization, and Integrated Discovery (DAVID) to obtain T2DM targets. Third, we constructed a network of the active component-target, target-pathway of DCHD using Cytoscape software (http://cytoscape.org/,ver.3.5.1) and then analyzed gene function, related biological processes, and signal pathways through the DAVID database. Results. We screened 77 active components from 1278 DCHD components and 116 effective targets from 253 ones. After matching the targets of T2DM, we obtained 38 important targets and 7 core targets were selected through further analysis. Through enrichment analysis, we found that these important targets were mainly involved in many biological processes such as oxidative stress, inflammatory reaction, and apoptosis. After analyzing the relevant pathways, the synthetic pathway for the treatment of T2DM was obtained, which provided a diagnosis-treatment idea for DCHD in the treatment of T2DM. Conclusions. This article reveals the mechanism of DCHD in the treatment of T2DM related to inflammatory response and apoptosis through network pharmacology, which lays a foundation for further elucidation of drugs effective targets.

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N-Myc-Interacting Protein Negatively Regulates TNF-α-Induced NF-κB Transcriptional Activity by Sequestering NF-κB/p65 in the Cytoplasm

Cited by 17 publications

References 51 publications

N‐myc and STAT interactor correlates with severity and prognosis in acute‐on‐chronic liver failure of hepatitis B virus

N‐myc and STAT interactor correlates with severity and prognosis in acute‐on‐chronic liver failure of hepatitis B virus

MiR-139-5p negatively regulates PMP22 to repress cell proliferation by targeting the NF-κB signaling pathway in gastric cancer

Integrated Analysis of the Mechanisms of Da‐Chai‐Hu Decoction in Type 2 Diabetes Mellitus by a Network Pharmacology Approach

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