1,8-cineol inhibits the Wnt/β-catenin signaling pathway through GSK-3 dephosphorylation in nasal polyps of chronic rhinosinusitis patients

Bruchhage, Karl‐Ludwig; Koennecke, M.; Drenckhan, Maren; Plötze-Martin, Kirstin; Pries, Ralph; Wollenberg, Barbara

doi:10.1016/j.ejphar.2018.07.060

Cited by 18 publications

(11 citation statements)

References 47 publications

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“…40 In the nasal polyps of chronic rhinosinusitis, 1,8-cineol modulated GSK-3b dephosphorylation to repress Wnt/b-catenin signaling. 41 In this study, we showed that miR-27a and p-GSK-3b/GSK-3b was highly expressed in breast cancer tissue compared with para-carcinoma tissue, and that there was a negative correlation between p-GSK-3b/GSK-3b and miR-27a. Different breast cancer cell lines were utilized to testify miR-27a and p-GSK-3b/ GSK-3b levels, and there was a significant difference in the BT-20 cell line compared with other cell lines.…”

Section: Discussionmentioning

confidence: 59%

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MiR-27a Facilitates Breast Cancer Progression via GSK-3β

Chen

Zhang

Cao

et al. 2020

Technol Cancer Res Treat

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Breast cancer remains one of the leading causes of cancer-associated death in women. MiR-27a is highly expressed in breast cancer tissue. However, the underlying mechanisms that promote breast cancer progression are unknown. In this study, we investigated the regulatory mechanisms of miR-27a and its target glycogen Synthase Kinase 3-β (GSK-3β) in breast cancer cells. We found that miR-27a was highly expressed in breast cancer tissues, which downregulated GSK-3β expression. We further identified GSK-3β as a direct target of miR-27a, and found that the miR-27a mediated suppression of GSK-3β activated Wnt/β-catenin-associated proliferative and invasive factor in breast cancer. The cell transfection assay demonstrated the overexpression of miR-27a also enhanced cell proliferation and invasion, and reduced cell apoptosis through GSK-3β. Finally, we demonstrated that the overexpression of miR-27a facilitated breast cancer progression through its ability to down-regulate the phosphorylation of GSK-3β both in vivo and vitro. These findings highlighted miR-27a as a novel therapeutic target in breast cancer.

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Section: Discussionmentioning

confidence: 59%

“… 40 In the nasal polyps of chronic rhinosinusitis, 1,8-cineol modulated GSK-3β dephosphorylation to repress Wnt/β-catenin signaling. 41 …”

Section: Discussionmentioning

confidence: 99%

MiR-27a Facilitates Breast Cancer Progression via GSK-3β

Chen

Zhang

Cao

et al. 2020

Technol Cancer Res Treat

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“…Specifically, Pourang et al found that patients with prevalent nasal polyposis are at an increased risk for malignancies of the head and neck, specifically squamous cell carcinoma, compared to individuals without nasal polyposis [16]. Moreover, TGF-β [17], Wnt [18], and Myc [19] pathways have been reported to be associated with CRSsNP and different cancers. is indicates that CRSwNP shares some common pathways with cancer.…”

Section: Discussionmentioning

confidence: 99%

Identification of Key Modules, Hub Genes, and Noncoding RNAs in Chronic Rhinosinusitis with Nasal Polyps by Weighted Gene Coexpression Network Analysis

Zhou

Zhen

Liu

et al. 2020

BioMed Research International

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Chronic rhinosinusitis with nasal polyps (CRSwNP) is a chronic inflammatory disease with relatively easy recurrence. However, the precise molecular mechanisms of this disease are poorly known. Based on gene sequencing data obtained from the Gene Expression Omnibus (GEO) database, we constructed coexpression networks by weighted gene coexpression network analysis (WGCNA). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed by the Database for Annotation, Visualization, and Integrated Discovery (DAVID). The core gene of pathogenesis, CRSwNP, was screened by protein-protein interaction data (PPI) from the HPRD database. Unsupervised clustering was applied to screen hub genes related to the phenotype of CRSwNP. Blue and turquoise modules were found to be most significantly related to the pathogenicity of CRSwNP. Functional enrichment analysis showed that cell proliferation in the blue modules, the apoptotic process in the turquoise module, and the cancer pathway in both modules were mostly significantly correlated with the development of CRSwNP. The noncoding RNAs (long noncoding RNA and microRNA) and the top 10 core genes in each module were found to be associated with the pathogenesis of CRSwNP. A total of nine hub genes were identified to be related to the CRSwNP phenotype. By qRT-PCR analysis, AKT1, CDH1, PIK3R1, CBL, LRP1, MALAT1, and XIST were proven to be associated with the pathogenesis of CRSwNP. AGR2, FAM3D, PIP, DSE, and TMC were identified to be related to the CRSwNP phenotype. Further exploration of these genes will reveal more important information about the mechanisms of CRSwNP.

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“…A high expression of phosphorylated GSK-3 was detected in the nasal polyp tissue of patients with CRSwNP compared with the healthy mucosa [40]. Recent studies have shown that the monoterpene oxide 1,8-cineol is able to negatively modulate the Wnt/β-catenin signaling pathway by GSK-3 dephosphorylation in nasal polyps of chronic rhinosinusitis patients [41]. The presence of Wnt, the loss of E-cadherin, and increased β-catenin are important molecular parameters that define the EMT process.…”

Section: Wnt Signaling Is Involved In Crswnpmentioning

confidence: 96%

Nasal Polyposis: Insights in Epithelial-mesenchymal Transition and Differentiation of Polyp Mesenchymal Stem Cells

Chiarella

Lombardo

Lobello

et al. 2020

Preprint

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Chronic rhinosinusitis is a common inflammatory disease of paranasal sinuses, which causes rhinorrhea, nasal congestion and hyposmia. The genetic predisposition or the exposure to irritants can sustain the inflammatory response and the development of nasal polyposis. Nasal polyps are benign and teardrop-shaped growths that project in the nasal cavities and originate from the ethmoid sinuses. This inflammatory process is associated with high expression of IL-5 cytokine and infiltration of eosinophils. Humanized monoclonal antibodies targeting IL-5 or its receptor, represent a therapeutic strategy in the treatment of nasal polyposis in combination with corticosteroids. The molecular pathogenesis of nasal polyps in CRS patients is associated to the epithelial-mesenchymal transition (EMT), a process in which epithelial cells lose their typical phenotype acquiring a mesenchymal phenotype. TGFβ/SMAD, ERK, and Wnt/β-catenin pathways are altered in EMT during the nasal tissue remodeling. miRNA and inhibitor molecules targeting these altered signaling pathways are able to interfere with EMT; which could lead to alternative therapies. Nasal polyps are an alternative source of mesenchymal stem cells which can be easily isolated from surgical biopsies. A molecular understanding of the biology of PO-MSCs will contribute to delineating inflammatory process underlying the development of nasal polyps.

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1,8-cineol inhibits the Wnt/β-catenin signaling pathway through GSK-3 dephosphorylation in nasal polyps of chronic rhinosinusitis patients

Cited by 18 publications

References 47 publications

MiR-27a Facilitates Breast Cancer Progression via GSK-3β

MiR-27a Facilitates Breast Cancer Progression via GSK-3β

Identification of Key Modules, Hub Genes, and Noncoding RNAs in Chronic Rhinosinusitis with Nasal Polyps by Weighted Gene Coexpression Network Analysis

Nasal Polyposis: Insights in Epithelial-mesenchymal Transition and Differentiation of Polyp Mesenchymal Stem Cells

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