NLRP3 inflammasome signaling as an early molecular response is negatively controlled by miR-186 in CFA-induced prosopalgia mice

Chen, Minglei; Kuang, Lin; Lin, Shu-kai

doi:10.1590/1414-431x20187602

Cited by 24 publications

(16 citation statements)

References 30 publications

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“…To further explore the mechanism of upstream signaling of Shp2, we predicted the targeting relationship between miR-186 and Shp2 through the website. It's reported that miR-186 inhibits the development of non-small lung cancer, colon cancer, cervical cancer and gastric cancer [27][28][29][30]. In our study, dual luciferase reporter assay confirmed that miR-186 negatively regulates Shp2 gene.…”

Section: Discussionsupporting

confidence: 78%

MiR-186 serves as a tumor suppressor in lung adenocarcinoma cells by down-regulation of Shp2 gene and inhibiting PI3K/Akt/mTOR signaling pathway

Yan

Zheng

et al. 2020

Preprint

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Background The study aimed to investigate the effect and mechanism of miR-186, which targets protein tyrosine phosphatase (Shp2) PI3K/Akt/mTOR signaling pathway, on the biological characteristics of lung adenocarcinoma cells. Methods In this experimental study, Human lung adenocarcinoma cell line SPC-A-1 was grouped as Blank group, negative control (NC) group, miR-186 mimic group, miR-186 inhibitor group, si-Shp2 group and miR-186 inhibitor+si-Shp2 group. Results The results showed that miR-186 can target and down-regulate the expression of Shp2 gene. Compared with the Blank group, levels of Shp2, N-cadherin and Bcl-2 and level of PI3K/p-PI3K, Akt/P-Akt, mTOR/p-mTOR as well as cell proliferation, migration and invasion ability and the proportion of cells in S phase significantly decreased in the miR-186 mimic group and the si-Shp2 group, while the levels of E-cadherin and Bax as well as the proportion of cells in G1 phase and cell gene and mediates apoptosis rate increased significantly (all P < 0.05). Compared with the miR-186 inhibitor group, the miR-186 inhibitor + si-Shp2 group showed similar trend in all parameters with the comparison above (all P < 0.05). Conclusions The overexpression of miR-186 can down-regulate Shp2 gene expression, further inhibit the proliferation, invasion and migration and promote apoptosis of lung adenocarcinoma cells by inhibiting the activation of PI3K/Akt/mTOR signaling pathway.

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Section: Discussionsupporting

confidence: 78%

MiR-186 serves as a tumor suppressor in lung adenocarcinoma cells by down-regulation of Shp2 gene and inhibiting PI3K/Akt/mTOR signaling pathway

Yan

Zheng

et al. 2020

Preprint

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“…Allergic symptoms of the mice, immune cell infiltration, cytokine levels, and NLRP3 inflammasome protein expression were reduced in the nasal mucosa after administration of modified miR-133b-3p mimics, indicating that miR-133b-3p downregulation may contribute to the pathogenesis of allergic rhinitis, whereas its upregulation shows therapeutic potential (56). In a mouse model of prosopalgia, miR-186-5p is downregulated, and injection of miRNA mimics could alleviate neuropathic pain behavior by downregulating NLRP3 expression and NLRP3 inflammasome activity (57). The levels of miR-495-3p are decreased in mice with myocardial ischemia/reperfusion injury, and by targeting NLRP3, treatment with miR-495-3p mimics alleviates inflammation (58).…”

Section: Mirnas Target Inflammasome Componentsmentioning

confidence: 99%

Dysregulation of Inflammasome Priming and Activation by MicroRNAs in Human Immune-Mediated Diseases

Boxberger

Hecker

Zettl

2019

The Journal of Immunology

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Inflammasomes are protein complexes that respond to a wide range of pathogens and cellular damage signals. Their activation prompts the caspase-1–mediated cleavage of the proinflammatory cytokines IL-1β and IL-18. Inflammasome dysregulation has been demonstrated to play a role in a range of diseases involving the adaptive immune system like multiple sclerosis, rheumatic diseases, and type 1 diabetes. Priming and activation of inflammasomes can be modulated by microRNAs (miRNAs), small noncoding RNAs that regulate gene expression posttranscriptionally. miRNAs, such as miR-223-3p, have been demonstrated to directly target the inflammasome components NLRP3, caspase-1, and caspase-8. Other miRNAs like miR-155-5p modulate TLR-, IL-1R–, TNFR-, and IFNAR-mediated signaling pathways upstream of the inflammasomes. In this study, we discuss how a more detailed elucidation of miRNA-driven inflammasome regulation helps in understanding the molecular processes underlying immune-mediated human diseases, holds potential for the identification of biomarkers and may offer novel targets for the development of future therapeutics.

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“…Studies have shown that miRNA186 can inhibit Interleukin-1β (IL-1β) expression by regulating NLRP3 inflammasome, suggesting that miRNA186 may participate in tumorigenesis by regulating the tumor microenvironment. 23 IL-1β plays a pro-inflammatory cytokine role involved in inflammatory responses, both acute and chronic. Multiple experiments in vitro and vivo have shown that IL-1β has a tumor-promoting effect and can promote lung cancer metastasis through adhesion, invasion, and tumor angiogenesis of lung cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Clinical Value of Serum and Exhaled Breath Condensate miR-186 and IL-1β Levels in Non-Small Cell Lung Cancer

Xie

Chen

et al. 2020

Technol Cancer Res Treat

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Objective: Our study aimed to investigate the expression level and clinical significance of serum and exhaled breath condensate miR-186 and IL-1β in non-small cell lung cancer patients. Methods: The serum and exhaled breath condensate specimens of 62 non-small cell lung cancer patients and 60 healthy controls were collected to detect miR-186 expression levels by real-time fluorescent quantitative PCR. Enzyme linked immunosorbent assay was applied to examine IL-1β concentration. Statistical analyses were used to evaluate the correlation between miR-186 and IL-1β in serum and clinicopathological features, traditional serum tumor markers, and inflammatory markers. The diagnostic efficacy of miR-186 and IL-1β for non-small cell lung cancer was evaluated by receiver operating characteristic curve analysis. The correlation between miR-186 and IL-1β was determined. Results: ① The relative expression level of miR-186 was greatly reduced in the serum and EBC of patients with non-small cell lung cancer, and the miR-186 expression level was reduced in different TNM stages of non-small cell lung cancer, from the early to later stages. ② The IL-1β concentration in serum and exhaled breath condensate of patients with non-small cell lung cancer was increased. ③ Serum miR-186 and IL-1β levels were closely related to lymph node metastasis, and the low expression of serum miR-186 and the high concentration of IL-1β were associated with higher serum carcinoembryonic antigen, C-reactive protein, and erythrocyte sedimentation rate levels. ④ ROC curve analysis showed that exhaled breath condensate miR-186 had higher area under the curve than serum miR-186, and the combined detection showed higher diagnostic efficacy than the separate detection. In addition, the combined detection of IL-1β and miR-186 has a larger AUC than the separate detection of both. ⑤ The correlation between serum miR-186 and IL-1β was negative. Conclusion: miR-186 and IL-1β are expected to be potential diagnostic biomarkers for non-small cell lung cancer.

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NLRP3 inflammasome signaling as an early molecular response is negatively controlled by miR-186 in CFA-induced prosopalgia mice

Cited by 24 publications

References 30 publications

MiR-186 serves as a tumor suppressor in lung adenocarcinoma cells by down-regulation of Shp2 gene and inhibiting PI3K/Akt/mTOR signaling pathway

MiR-186 serves as a tumor suppressor in lung adenocarcinoma cells by down-regulation of Shp2 gene and inhibiting PI3K/Akt/mTOR signaling pathway

Dysregulation of Inflammasome Priming and Activation by MicroRNAs in Human Immune-Mediated Diseases

Clinical Value of Serum and Exhaled Breath Condensate miR-186 and IL-1β Levels in Non-Small Cell Lung Cancer

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