scholarly journals The Cell Adhesion Molecule Echinoid Functions as a Tumor Suppressor and Upstream Regulator of the Hippo Signaling Pathway

2012 ◽  
Vol 22 (2) ◽  
pp. 255-267 ◽  
Author(s):  
Tao Yue ◽  
Aiguo Tian ◽  
Jin Jiang
Keyword(s):  
Cell Adhesion ◽  
Tumor Suppressor ◽  
Signaling Pathway ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Hippo Signaling ◽  
Hippo Signaling Pathway ◽  
Upstream Regulator

scholarly journals MIR502 Acts As a Tumor Suppressor Gene to Accelerate Apoptosis and Suppress Proliferation by Targeting Hippo Signaling Pathway in Ovarian Cancer

2020 ◽  
Author(s):  
Yan Li ◽  
Qi Wang ◽  
Ning Ning ◽  
Fanglan Tang ◽  
Yan Wang
Keyword(s):  
Ovarian Cancer ◽  
Signaling Pathway ◽  
Kegg Pathway ◽  
Enrichment Analysis ◽  
Suppressor Gene ◽  
Hippo Signaling ◽  
Ppi Network ◽  
Pathway Enrichment ◽  
Hippo Signaling Pathway ◽  
Upstream Regulator

Abstract Background Ovarian cancer (OC) is the major cause of death among women due to the lack of early screening methods and complex pathological progression. Increasing evidence indicated that microRNAs were considered as gene expression regulators in tumors by interacting with mRNAs. Although researches regarding with OC and microRNAs are extensive, the vital role of MIR502 in OC still remains unclear.Methods We integrated two microRNA expression arrays from GEO to identify differentially expressed genes. Kaplan–Meier method was used to screen miRNAs that had influence on survival outcome. Upstream regulator of MIR502 was predicted by JASPAR and verified by ChIP-seq data. The LinkedOmics database was used to study correlated genes with MIR502. Gene Set Enrichment Analysis (GSEA) was conducted to reveal the functional annotation of GO and KEGG pathway enrichment analysis by using the open access WebGestalt tool. We constructed PPI network by using the STRING to further explore core protein.Results We found that expression level of MIR502 was significantly down regulated in OC, which was related to poor overall survival outcome. NRF1 as the upstream regulator of MIR502 was predicted by JASPAR and verified by ChIP-seq data. In addition, anti-apoptosis and pro-proliferation genes attending in Hippo signaling pathway, including CCND1, MYC, FGF1 and GLI2 were negatively regulated by MIR502 in the analysis of GO and KEGG pathway enrichment results. PPI network further demonstrated that CCND1 and MYCN were at core position in the development of ovarian cancer.Conclusions MIR502, which was regulated by NRF1, acted as a tumor suppressor gene to accelerate apoptosis and suppress proliferation by targeting Hippo signaling pathway in ovarian cancer.

Axonal Guidance Signaling Pathway Is Suppressed in Human Nasal Polyps

2018 ◽  
Vol 32 (4) ◽  
pp. 208-216 ◽  
Author(s):  
Dawei Wu ◽  
Sarina K. Mueller ◽  
Angela L. Nocera ◽  
Kristen Finn ◽  
Towia A. Libermann ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Adhesion Molecule ◽  
Nasal Polyps ◽  
Cell Adhesion Molecule ◽  
Neuronal Cell ◽  
Axonal Guidance ◽  
Axonal Outgrowth ◽  
Neuronal Growth

Background Dysfunctional innervation might contribute to the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP), but the state of the axonal outgrowth signaling in CRSwNP is unknown. The purpose of this study was to explore the axonal outgrowth pathway-related protein expression in CRSwNP. Methods Institutional review board approved study in which tissue proteomes were compared between control and CRSwNP patients (n = 10/group) using an aptamer-based proteomic array and confirmed by whole transcriptomic analysis. Results Compared with controls, proteins associated with axonal guidance signaling pathway such as beta-nerve growth factor, semaphorin 3A, Ras-related C3 botulinum toxin substrate 1, Bcl-2, protein kinase C delta type, and Fyn were significantly decreased in patients with CRSwNP (fold change [FC] = −1.17, P = .002; FC = −1.09, P < .001; FC = −1.33, P < .001; FC = −1.31, P < .001; FC = −1.31, P = .004; and FC = −1.20, P = 0.012, respectively). In contrast, reticulon-4 receptor, an inhibitory factor, was significantly increased in patients with CRSwNP (FC = 1.25, P < .001). Furthermore, neuronal growth-associated proteins such as ciliary neurotrophic factor receptor subunit alpha, neuronal growth regulator 1, neuronal cell adhesion molecule, neural cell adhesion molecule L1, platelet-derived growth factor subunit A, and netrin-4 were all significantly decreased in patients with CRSwNP (FC = −1.25, P < .001; FC = −1.27, P = .002; FC = −1.65, P = .013; FC = −4.20, P < .001; FC = −1.28, P < .001; and FC = −2.31, P < .001, respectively). In contrast, tissue eosinophil count ( P < .001) and allergic inflammation factors such as IgE, periostin, and galectin-10 were all significantly increased in patients with CRSwNP (FC = 12.28, P < .001; FC = 3.95, P < .001; and FC = 2.44, P < .001, respectively). Furthermore, the log FC of the studied proteins expression significantly and positively correlated with log FC of their mRNA expression ( P < .001, r = .88). Conclusions Axonal guidance signaling and neural growth factors pathways proteins are significantly suppressed in eosinophilic CRSwNP.

Generation of a monoclonal antibody specific to a new candidate tumor suppressor, cell adhesion molecule 2

Tumor Biology ◽  
2014 ◽  
Vol 35 (8) ◽  
pp. 7415-7422 ◽  
Author(s):  
Meijin Huang ◽  
Ziyuan Xia ◽  
Yang Wang ◽  
Liang Huang ◽  
Qian Ma ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Cell Adhesion ◽  
Tumor Suppressor ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Suppressor Cell ◽  
Candidate Tumor Suppressor

Dysregulated CREB signaling pathway in the brain of neural cell adhesion molecule (NCAM)-deficient mice

2008 ◽  
Vol 1243 ◽  
pp. 104-112 ◽  
Author(s):  
Anu Aonurm-Helm ◽  
Tamara Zharkovsky ◽  
Monika Jürgenson ◽  
Anti Kalda ◽  
Alexander Zharkovsky
Keyword(s):  
Cell Adhesion ◽  
Signaling Pathway ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Neural Cell Adhesion Molecule ◽  
Neural Cell ◽  
Neural Cell Adhesion ◽  
The Brain ◽  
Deficient Mice
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