Tumor-derived fibulin-3 activates pro-invasive NF-κB signaling in glioblastoma cells and their microenvironment

Nandhu, Mohan S.; Kwiatkowska, Aneta; Bhaskaran, Vivek; Hayes, Josie; Hu, Bin; Viapiano, Mariano S.

doi:10.1038/onc.2017.109

Cited by 32 publications

(26 citation statements)

References 66 publications

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“…[33][34][35][36] However, in human gliomas, EFEMP1 was significantly up-regulated and promoted tumor cell motility and invasion with elevated expression and activity of matrix metalloproteases, such as MMP-2, MMP-9, ADAMTS-5 and ADAM17. [37][38][39] In conclusion, there are reports for prooncogenic and anti-oncogenic roles for EFEMP2, and more in-depth research is needed in the future.…”

Section: Discussionmentioning

confidence: 94%

<p>EFEMP2 Suppresses the Invasion of Lung Cancer Cells by Inhibiting Epithelial-Mesenchymal Transition (EMT) and Down-Regulating MMPs</p>

Song¹,

Li²,

Liu³

et al. 2020

OTT

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Background: Epidermal growth factor-containing fibulin-like extracellular matrix protein 2 (EFEMP2), also known as fibulin-4, MBP1 and UPH1, is an extracellular matrix protein associated with a variety of tumors. The purpose of this study was to investigate the prognostic value and the function of EFEMP2 in lung cancer. Methods: The mRNA and protein expression of EFEMP2 in lung normal and cancer tissues, lung cancer cell lines (A549, H460, H1299 and H1650) and normal epithelial cell line BEAS-2B were evaluated by immunohistochemistry, RT-qPCR and Western blotting. The Public databases (Oncomine and Kaplan-Meier plotter) were used to investigate the prognostic value of EFEMP2 in lung cancer. RNA interference (RNAi) and overexpression transfection were performed to detect the effects of EFEMP2 up-or down-regulation on lung normal and cancer cell proliferation, invasion and metastasis in vitro and in vivo. Results: EFEMP2 was lowly expressed in lung cancer tissues and cells, and its low expression was associated with malignant phenotype and poor prognosis of lung cancer. The same conclusion had been drawn from the Public databases. EFEMP2 overexpression significantly inhibited the invasion of lung cancer cells, hampered the process of EMT, and decreased the expression and activity of MMP2 and MMP9, while EFEMP2 knockdown remarkably enhanced the invasion of lung cancer cells, promoted EMT, and increased the expression and activity of MMP2 and MMP9. Conclusion: The low expression of EFEMP2 was detected in lung cancer and was positively correlated with the poor prognosis of patients. EFEMP2 was a tumor suppressor gene that inhibited the progress of lung cancer, which suggested a new research objective for the future studies.

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Section: Discussionmentioning

confidence: 94%

<p>EFEMP2 Suppresses the Invasion of Lung Cancer Cells by Inhibiting Epithelial-Mesenchymal Transition (EMT) and Down-Regulating MMPs</p>

Song¹,

Li²,

Liu³

et al. 2020

OTT

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“…BAY 11-7082 is a specific pharmacologic NF-κB inhibitor with obvious cytotoxicity, which leads to increasing cell death as the concentration increases [87]. Some studies have shown that BAY 11-7082 impairs alveolar epithelial barrier function and causes unavoidable toxicity in cells and cultured brain tissue [88,89]. In the application of BAY 11-7085 system, toxic reactions were detected, so the local application of NF-κB inhibitor was paid more attention by many scholars.…”

Section: Therapeutic Prospects Of Targeting Inflammasomes In Renal DImentioning

confidence: 99%

Research Progress on the Role of Inflammasomes in Kidney Disease

Chi

Geng

Liu

et al. 2020

Mediators of Inflammation

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Inflammasomes are multimeric complexes composed of cytoplasmic sensors, apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC or PYCARD), and procaspase-1 and play roles in regulating caspase-dependent inflammation and cell death. Inflammasomes are assembled by sensing pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) and initiate inflammatory responses by activating caspase-1. Activated caspase-1 promotes the release of the inflammatory cytokines interleukin-1β (IL-1β) and IL-18 and eventually induces pyroptosis. Inflammasomes are closely related to kidney diseases. In particular, the NLRP3 (NACHT, LRR, and PYD domain-containing protein 3) inflammasome has been shown to cause acute and chronic kidney diseases by regulating canonical and noncanonical mechanisms of inflammation. Small-molecule inhibitors that target NLRP3 and other components of the inflammasome are potential options for the treatment of kidney-related diseases such as diabetic nephropathy. This article will focus on the research progress on inflammasomes and the key pathogenic roles of inflammasomes in the development and progression of kidney diseases and explore the potential of this intracellular inflammation to further prevent or block the development of the kidney disease.

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“…Ultimately, the Fibulin-3 is an extracellular protein described to be released by GB cells, and its expression is associated with tumor invasiveness and proliferation. Besides, an in vivo study showed that in the core and border of fibulin-3-overexpressed GB occurs the activation of NF-κB in p65+ astrocytes and GB cells ( Nandhu et al, 2017 ).…”

Section: Microglia and Astrocytes’ Role In Glioblastoma Malignancymentioning

confidence: 99%

Microglia/Astrocytes–Glioblastoma Crosstalk: Crucial Molecular Mechanisms and Microenvironmental Factors

Matias

Balça-Silva

Graça

et al. 2018

Front. Cell. Neurosci.

130

120

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In recent years, the functions of glial cells, namely, astrocytes and microglia, have gained prominence in several diseases of the central nervous system, especially in glioblastoma (GB), the most malignant primary brain tumor that leads to poor clinical outcomes. Studies showed that microglial cells or astrocytes play a critical role in promoting GB growth. Based on the recent findings, the complex network of the interaction between microglial/astrocytes cells and GB may constitute a potential therapeutic target to overcome tumor malignancy. In the present review, we summarize the most important mechanisms and functions of the molecular factors involved in the microglia or astrocytes–GB interactions, which is particularly the alterations that occur in the cell’s extracellular matrix and the cytoskeleton. We overview the cytokines, chemokines, neurotrophic, morphogenic, metabolic factors, and non-coding RNAs actions crucial to these interactions. We have also discussed the most recent studies regarding the mechanisms of transportation and communication between microglial/astrocytes – GB cells, namely through the ABC transporters or by extracellular vesicles. Lastly, we highlight the therapeutic challenges and improvements regarding the crosstalk between these glial cells and GB.

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Tumor-derived fibulin-3 activates pro-invasive NF-κB signaling in glioblastoma cells and their microenvironment

Cited by 32 publications

References 66 publications

<p>EFEMP2 Suppresses the Invasion of Lung Cancer Cells by Inhibiting Epithelial-Mesenchymal Transition (EMT) and Down-Regulating MMPs</p>

<p>EFEMP2 Suppresses the Invasion of Lung Cancer Cells by Inhibiting Epithelial-Mesenchymal Transition (EMT) and Down-Regulating MMPs</p>

Research Progress on the Role of Inflammasomes in Kidney Disease

Microglia/Astrocytes–Glioblastoma Crosstalk: Crucial Molecular Mechanisms and Microenvironmental Factors

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