RAGE and AXL expression following secondhand smoke (SHS) exposure in mice

Tsai, Kary Y F; Budge, Kelsey M Hirschi; Llavina, S.; Davis, Taylor; Long, Matt; Bennett, Abby; Sitton, Beau; Arroyo, Juan A.; Reynolds, Paul

doi:10.1080/01902148.2019.1684596

Cited by 7 publications

(10 citation statements)

References 62 publications

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“…ATG7, an autophagic gene, is increasingly activated in the early stages of lung injury induced by cigarette smoke [35,36]. AXL is a receptor tyrosine kinase related to cancer and immune function, which mediates signal transduction related to proliferation and inflammation [37]. During secondhand smoke, the interaction between AXL and receptors for advanced glycation end products can cause COPD.…”

Section: Discussionmentioning

confidence: 99%

The benefits of smoking cessation on survival in cancer patients by integrative analysis of multi‐omics data

2020

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Few studies have examined the association between smoking status (including former smokers) at diagnosis and overall survival among cancer patients. We aimed to assess the benefits of quitting smoking on cancer prognosis in cohorts of cancer patient smokers obtained from the Cancer Genome Atlas (TCGA) database. Hazard ratios (HR) were calculated to evaluate smoking behavior at cancer diagnosis (reformed smokers vs. current smokers) in association with overall survival using multivariate‐adjusted Cox regressions analysis. According to our analyses, quitting smoking was the independent protective factor for overall survival in lung squamous cell carcinoma (LUSC) (HR = 0.67, 95% CI = 0.48–0.94). Comprehensive analysis of multicomponent data across reformed and current smokers identified a total of 85 differential expressed genes (DEGs) affected by different modes of genetic and epigenetic regulation, potentially representing cancer drivers in smokers. Moreover, we provided a smoking‐associated gene expression signature, which could evaluate the true effect on prognosis with high power (HR = 1.70, 95% CI = 1.19–2.43, AUC = 0.65, 0.67, and 0.70 for 2‐, 3‐, and 5‐year survival, respectively). This signature was also applicable in other smoking‐related cancers, including bladder urothelial carcinoma (HR = 1.70, 95% CI = 1.01–2.88), cervical carcinoma (HR = 5.69, 95% CI = 1.37–23.69), head and neck squamous cell carcinoma (HR = 1.97, 95% CI = 1.41–2.76), lung adenocarcinoma (HR = 1.73, 95% CI = 1.16–2.57), and pancreatic adenocarcinoma (HR = 4.28, 95% CI = 1.47–12.47). In conclusion, this study demonstrates that quitting smoking at diagnosis decreases risk of death in cancer patients. We also provide a smoking‐associated gene expression signature to evaluate the effect of smoking on survival. Lastly, we suggest that smoking cessation could comprise a part of cancer treatment to improve survival rates of cancer patients.

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Section: Discussionmentioning

confidence: 99%

The benefits of smoking cessation on survival in cancer patients by integrative analysis of multi‐omics data

2020

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“…ATG7, an autophagic gene, is increasingly activated in the early stages of lung injury induced by cigarette smoke (38,39). AXL is a receptor tyrosine kinase related to cancer and immune function, which mediates signal transduction related to proliferation and inflammation (40). During secondhand smoke, the interaction between AXL and receptors for advanced glycation end-products to cause COPD.…”

Section: Discussionmentioning

confidence: 99%

The benefits of smoking cessation on survival in cancer patients by integrative analysis of multi-omics data

Yang¹,

Liu²,

Liang³

2020

Preprint

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Background: Few studies have examined the association between smoking cessation at the time of diagnosis and overall survival among cancer patients. We aimed to assess the benefits of quitting smoking on prognosis.Methods: We obtained cohorts of smoking-related cancer patients from the Cancer Genome Atlas (TCGA) database. Hazard ratios (HR) with 95% confidence intervals (CIs) were calculated to evaluate smoking behavior at cancer diagnosis (reformed smokers vs. current smokers) in association with overall survival using age and multivariate-adjusted Cox regressions analysis. Comprehensive analysis of multi-component data was carried out to determine the genetic and epigenetic landscape differences and their effects on the differential expression genes (DEGs) between reformed smokers and current smokers. The smoking signature was constructed using univariate Cox regression and LASSO-Cox regression model.Results: According to the multivariate-adjusted Cox regressions analysis, quitting smoking was the independent protective factor for overall survival in lung squamous cell carcinoma (LUSC) (HR=0.67, 95%CI=0.48-0.94). A total of 85 key DEGs were found to be affected by different modes of genetic and epigenetic regulation, which might represent key drivers in smokers. At last, we provided the smoking signature which could predict prognosis with high power (HR=1.70, 95% CI=1.19-2.43, AUC= 0.65, 0.67 and 0.70 for 2, 3 and 5-year survival, respectively). The smoking signature was also applicable in other smoking-related cancers, including bladder urothelial carcinoma (HR=1.70, 95% CI=1.01-2.88), cervical carcinoma (HR=5.69, 95% CI=1.37-23.69), head and neck squamous cell carcinoma (HR=1.97, 95% CI=1.41-2.76), lung adenocarcinoma (HR=1.73, 95% CI=1.16-2.57), and pancreatic adenocarcinoma (HR=4.28, 95% CI=1.47-12.47).Conclusions: The present study demonstrated that quitting smoking at diagnosis decreased risk of death in cancer patients. We also provided the smoking signature to evaluate the true effect of smoking, suggesting that smoking cessation could be a part of cancer treatment to improve the survival rate of cancer patients.

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“…With regards to the potential therapeutic role of GAGs in COPD, in a murine model of smoke-induced lung disease, treatment with intraperitoneal polysulphated HA reduced BAL IL-1α, IL-2, and TNFα levels, with reduced BAL inflammation and lung permeability recorded [ 101 ]. Indeed, investigations into the therapeutic anti-inflammatory properties of high-molecular-weight HA in COPD, included an in vitro study demonstrating that HA had a protective effect on lung elasticity by preventing elastolysis [ 99 ].…”

Section: The Role Of Glycosaminoglycans In Airways Diseasementioning

confidence: 99%

Targeting of Glycosaminoglycans in Genetic and Inflammatory Airway Disease

Caird

Williamson

Yusuf

et al. 2022

IJMS

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In the lung, glycosaminoglycans (GAGs) are dispersed in the extracellular matrix (ECM) occupying the interstitial space between the capillary endothelium and the alveolar epithelium, in the sub-epithelial tissue and in airway secretions. In addition to playing key structural roles, GAGs contribute to a number of physiologic processes ranging from cell differentiation, cell adhesion and wound healing. Cytokine and chemokine–GAG interactions are also involved in presentation of inflammatory molecules to respective receptors leading to immune cell migration and airway infiltration. More recently, pathophysiological roles of GAGs have been described. This review aims to discuss the biological roles and molecular interactions of GAGs, and their impact in the pathology of chronic airway diseases, such as cystic fibrosis and chronic obstructive pulmonary disease. Moreover, the role of GAGs in respiratory disease has been heightened by the current COVID-19 pandemic. This review underlines the essential need for continued research aimed at exploring the contribution of GAGs in the development of inflammation, to provide a better understanding of their biological impact, as well as leads in the development of new therapeutic agents.

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RAGE and AXL expression following secondhand smoke (SHS) exposure in mice

Cited by 7 publications

References 62 publications

The benefits of smoking cessation on survival in cancer patients by integrative analysis of multi‐omics data

The benefits of smoking cessation on survival in cancer patients by integrative analysis of multi‐omics data

The benefits of smoking cessation on survival in cancer patients by integrative analysis of multi-omics data

Targeting of Glycosaminoglycans in Genetic and Inflammatory Airway Disease

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