LncRNA NEAT1 Promotes Inflammatory Response in Sepsis via the miR-31-5p/POU2F1 Axis

Abstract Sepsis is considered to be a systemic inflammatory response, which results in organ dysfunction. LncRNA nuclear-enriched abundant transcript 1 (NEAT1) involved in sepsis progression has been reported. However, the underlying mechanism of NEAT1 in sepsis-induced inflammatory response remains to be revealed. In this study, NEAT1 and POU domain class 2 transcription factor 1 (POU2F1) were highly expressed in LPS-induced septic RAW264.7 cells, opposite to miR-31-5p expression. Furthermore, we found that NEAT1 silencing inhibited LPS-induced inflammatory response and cell proliferation, and promoted cell apoptosis. Subsequently, we found that miR-31-5p interacted with NEAT1 and targeted the 3′UTR of POU2F1, and in LPS-induced RAW264.7 cells, the inhibition of NEAT1 silencing was reversed by miR-31-5p knockdown, while POU2F1 downregulation could cover the functions of miR-31-5p knockdown. In a word, this study indicates that NEAT1 inhibits the LPS-induced progression of sepsis in RAW264.7 cells by modulating miR-31-5p/POU2F1 axis, suggesting that NEAT1 will be the potential therapeutic target for sepsis.

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Novel small molecular inhibitor of Pit-Oct-Unc transcription factor 1 suppresses hepatocellular carcinoma cell proliferation

Life Sciences ◽

10.1016/j.lfs.2021.119521 ◽

2021 ◽

pp. 119521

Author(s):

Yue Wang ◽

Shuo Liu ◽

Qin Chen ◽

Yixin Ren ◽

Zhongxiang Li ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Cell Proliferation ◽

Transcription Factor ◽

Carcinoma Cell ◽

Hepatocellular Carcinoma Cell ◽

Transcription Factor 1

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Upregulation of miR-150-5p alleviates LPS-induced inflammatory response and apoptosis of RAW264.7 macrophages by targeting Notch1

Open Life Sciences ◽

10.1515/biol-2020-0058 ◽

2020 ◽

Vol 15 (1) ◽

pp. 544-552

Author(s):

Xiaoyan Deng ◽

Zhixing Lin ◽

Chao Zuo ◽

Yanjie Fu

Keyword(s):

Inflammatory Response ◽

Underlying Mechanism ◽

Notch Receptor ◽

Raw264.7 Cells ◽

Luciferase Reporter ◽

Raw264.7 Macrophages ◽

Factor Α ◽

Anti Inflammation ◽

Necrosis Factor ◽

Dual Luciferase Reporter Assay

AbstractCirculating miR-150-5p has been identified as a prognostic marker in patients with critical illness and sepsis. Herein, we aimed to further explore the role and underlying mechanism of miR-150-5p in sepsis. Quantitative real-time-PCR assay was performed to detect the expression of miR-150-5p upon stimulation with lipopolysaccharide (LPS) in RAW264.7 cells. The levels of tumor necrosis factor-α, interleukin (IL)-6 and IL-1β were measured by ELISA assay. Cell apoptosis was determined using flow cytometry. Western blot was used to assess notch receptor 1 (Notch1) expression in LPS-induced RAW264.7 cells. Dual-luciferase reporter assay was employed to validate the target of miR-150-5p. Our data showed that miR-150-5p was downregulated and Notch1 was upregulated in LPS-stimulated RAW264.7 cells. miR-150-5p overexpression or Notch1 silencing alleviated LPS-induced inflammatory response and apoptosis in RAW264.7 cells. Moreover, Notch1 was a direct target of miR-150-5p. Notch1 abated miR-150-5p-mediated anti-inflammation and anti-apoptosis in LPS-induced RAW264.7 cells. miR-150-5p alleviated LPS-induced inflammatory response and apoptosis at least partly by targeting Notch1 in RAW264.7 cells, highlighting miR-150-5p as a target in the development of anti-inflammation and anti-apoptosis drugs for sepsis treatment.

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MicroRNA-200c promotes tumor cell proliferation and migration by directly targeting dachshund family transcription factor 1 by the Wnt/β-catenin signaling pathway in nasopharyngeal carcinoma

Anti-Cancer Drugs ◽

10.1097/cad.0000000000000713 ◽

2019 ◽

Vol 30 (3) ◽

pp. 218-224 ◽

Cited By ~ 5

Author(s):

Wei Cao ◽

Jingwu Sun

Keyword(s):

Cell Proliferation ◽

Transcription Factor ◽

Nasopharyngeal Carcinoma ◽

Tumor Cell ◽

Signaling Pathway ◽

Tumor Cell Proliferation ◽

Cell Proliferation And Migration ◽

And Migration ◽

Transcription Factor 1 ◽

Proliferation And Migration

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Brn-2 Expression Controls Melanoma Proliferation and Is Directly Regulated by β-Catenin

Molecular and Cellular Biology ◽

10.1128/mcb.24.7.2915-2922.2004 ◽

2004 ◽

Vol 24 (7) ◽

pp. 2915-2922 ◽

Cited By ~ 82

Author(s):

Jane Goodall ◽

Silvia Martinozzi ◽

Timothy J. Dexter ◽

Delphine Champeval ◽

Suzanne Carreira ◽

...

Keyword(s):

Cell Proliferation ◽

Transcription Factor ◽

Signaling Pathway ◽

Target Genes ◽

Constitutive Activation ◽

Pou Domain ◽

Common Cancer ◽

Interfering Rna ◽

Melanoma Cell Lines

ABSTRACT Constitutive activation of the Wnt/β-catenin signaling pathway is a notable feature of a large minority of cases of malignant melanoma, an aggressive and increasingly common cancer. The identification of target genes downstream from this pathway is therefore crucial to our understanding of the disease. The POU domain transcription factor Brn-2 has been implicated in control of proliferation and melanoma survival, and its expression is strongly upregulated in melanoma. We show here that in vivo Brn-2 is expressed in melanocytes but not in embryonic day 11.5 melanoblasts and that its expression is directly controlled by the Wnt/β-catenin signaling pathway in melanoma cell lines and in transgenic mice. Moreover, silent interfering RNA-mediated inhibition of Brn-2 expression in melanoma cells overexpressing β-catenin results in significantly decreased proliferation. These results, together with the observation that BRAF signaling also induces Brn-2 expression, reveal that Brn-2 is a focus for the convergence of two key melanoma-associated signaling pathways that are linked to cell proliferation.

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