RAGE may act as a tumour suppressor to regulate lung cancer development

Wu, Shuangshuang; Mao, Liping; Li, Yan; Yin, Yuan; Yuan, Weiwei; Chen, Yujia; Ren, Wenlong; Lü, Xiao; Li, Yue; Chen, Lei; Chen, Bin; Xu, Wei; Tian, Tian; Lu, Yihua; Jiang, Liying; Zhuang, Xun; Chu, Minjie; Wu, Jianqing

doi:10.1016/j.gene.2018.02.009

Cited by 14 publications

(11 citation statements)

References 25 publications

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“…AGER is a multi-ligand receptor that binds various ligands derived from a damaged cell and its up-regulation at both mRNA and protein level is associated with the majority of cancers including gastric, breast, hepatocellular, colorectal carcinoma (44, 45). However, unlike other cancers, AGER is down-regulated in NSCLC and also supported by the previous finding suggested its role as a tumor suppressor in lung cancer (46). S100A12 is a small protein express by neutrophil granulocytes and binds with AGER receptor, which induces the production of proinflammatory cytokines (47).…”

Section: Discussionsupporting

confidence: 67%

Integrated Network Analysis Reveals FOXM1 and MYBL2 as Key Regulators of Cell Proliferation in Non-small Cell Lung Cancer

Ahmed

2019

Front. Oncol.

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Background: Loss of control on cell division is an important factor for the development of non-small cell lung cancer (NSCLC), however, its molecular mechanism and gene regulatory network are not clearly understood. This study utilized the systems bioinformatics approach to reveal the “driver-network” involve in tumorigenic processes in NSCLC.Methods: A meta-analysis of gene expression data of NSCLC was integrated with protein-protein interaction (PPI) data to construct an NSCLC network. MCODE and iRegulone were used to identify the local clusters and its upstream transcription regulators involve in NSCLC. Pair-wise gene expression correlation was performed using GEPIA. The survival analysis was performed by the Kaplan-Meier plot.Results: This study identified a local “driver-network” with highest MCODE score having 26 up-regulated genes involved in the process of cell proliferation in NSCLC. Interestingly, the “driver-network” is under the regulation of TFs FOXM1 and MYBL2 as well as miRNAs. Furthermore, the overexpression of member genes in “driver-network” and the TFs are associated with poor overall survival (OS) in NSCLC patients.Conclusion: This study identified a local “driver-network” and its upstream regulators responsible for the cell proliferation in NSCLC, which could be promising biomarkers and therapeutic targets for NSCLC treatment.

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Section: Discussionsupporting

confidence: 67%

Integrated Network Analysis Reveals FOXM1 and MYBL2 as Key Regulators of Cell Proliferation in Non-small Cell Lung Cancer

Ahmed

2019

Front. Oncol.

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“…Another eGene AGER is expressed primarily in the lung and has polymorphisms that may potentially increase the risk of lung cancer [84]. Detecting AGER as eGene agrees with the previous finding of the association between lung cancer and PM/DM [85]. Collectively, our analysis successfully captured several known genes implicated in complications of PM and DM patients, which may validate the soundness of our study.…”

Section: Discussionsupporting

confidence: 84%

“…All eGenes in Table 3 and Table 4 have been previously mentioned to have a positive correlation with malignancy or some other severe complication of PM and DM [75,76,77,78,79,80,81,82,83,84,85]. NF-κB signaling and zinc finger proteins are known for their activity in key mechanisms of cancers such as migration, autophagy, apoptosis, cytokine processing, and metastasis [76,77,78,79].…”

Section: Discussionmentioning

confidence: 99%

Meta-Analysis of Polymyositis and Dermatomyositis Microarray Data Reveals Novel Genetic Biomarkers

Song

Kim

Hong

et al. 2019

Genes

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Polymyositis (PM) and dermatomyositis (DM) are both classified as idiopathic inflammatory myopathies. They share a few common characteristics such as inflammation and muscle weakness. Previous studies have indicated that these diseases present aspects of an auto-immune disorder; however, their exact pathogenesis is still unclear. In this study, three gene expression datasets (PM: 7, DM: 50, Control: 13) available in public databases were used to conduct meta-analysis. We then conducted expression quantitative trait loci analysis to detect the variant sites that may contribute to the pathogenesis of PM and DM. Six-hundred differentially expressed genes were identified in the meta-analysis (false discovery rate (FDR) < 0.01), among which 317 genes were up-regulated and 283 were down-regulated in the disease group compared with those in the healthy control group. The up-regulated genes were significantly enriched in interferon-signaling pathways in protein secretion, and/or in unfolded-protein response. We detected 10 single nucleotide polymorphisms (SNPs) which could potentially play key roles in driving the PM and DM. Along with previously reported genes, we identified 4 novel genes and 10 SNP-variant regions which could be used as candidates for potential drug targets or biomarkers for PM and DM.

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“…In the medical literature, a growing number of studies have shown that RAGE plays a critical role in physiological and pathological processes of the lungs, and variants in RAGE gene may predispose to the risk of respiratory disorders, including COPD and asthma [36–39]. However, the results of most published studies remain inconsistent and inconclusive, with no consensus on genetic implications of RAGE gene, likely due to ethnic diversity of genetic backgrounds, lack of adjustment for confounders and disregard of haplotype analyses.…”

Section: Discussionmentioning

confidence: 99%

Association of RAGE gene multiple variants with the risk for COPD and asthma in northern Han Chinese

Niu

et al. 2019

Aging

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Clinical and experimental data have shown that the receptor for advanced glycation end products (RAGE) is implicated in the pathogenesis of respiratory disorders. In this study, we genotyped five widely-evaluated variants in RAGE gene, aiming to assess their association with the risk for chronic obstructive pulmonary disease (COPD) and asthma in northern Han Chinese. Genotypes were determined in 105 COPD patients, 242 asthma patients and 527 controls. In single-locus analysis, there was significant difference in the genotype distributions of rs1800624 between COPD patients and controls ( p =0.022), and the genotype and allele distributions of rs1800625 differed significantly ( p =0.040 and 0.016) between asthma patients and controls. Haplotype analysis revealed that haplotype T-A-G-T (allele order: rs1800625, rs1800624, rs2070600, rs184003) was significantly associated with a reduced COPD risk (OR=0.32, 95% CI: 0.06-0.60), and haplotype T-A-A-G was significantly associated with a reduced asthma risk (OR=0.19, 95% CI: 0.04-0.96). Further haplotype-phenotype analysis showed that high- and low-density lipoprotein cholesterol and blood urea nitrogen were significant mediators for COPD ( p sim =0.041, 0.043 and 0.030, respectively), and total cholesterol was a significant mediator for asthma ( p sim =0.009). Taken together, our findings indicate that RAGE gene is a promising candidate for COPD and asthma, and importantly both disorders are genetically heterogeneous.

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RAGE may act as a tumour suppressor to regulate lung cancer development

Cited by 14 publications

References 25 publications

Integrated Network Analysis Reveals FOXM1 and MYBL2 as Key Regulators of Cell Proliferation in Non-small Cell Lung Cancer

Integrated Network Analysis Reveals FOXM1 and MYBL2 as Key Regulators of Cell Proliferation in Non-small Cell Lung Cancer

Meta-Analysis of Polymyositis and Dermatomyositis Microarray Data Reveals Novel Genetic Biomarkers

Association of RAGE gene multiple variants with the risk for COPD and asthma in northern Han Chinese

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