Cigarette smoke extract induces oral squamous cell carcinoma cell invasion in a receptor for advanced glycation end‐products‐dependent manner

Chapman, Steven; Mick, Madison; Hall, Parker; Mejía, Camilo A.; Sue, Stephanie; Wase, Bihishta Abdul; Nguyen, Margaret A.; Whisenant, Evan C.; Wilcox, Shalene H.; Winden, Duane R.; Reynolds, Paul; Arroyo, Juan A.

doi:10.1111/eos.12395

Cited by 17 publications

(24 citation statements)

References 42 publications

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“…Advanced glycation end-products (AGE) are formed from reducing sugars and biomolecules such as proteins, lipids, and nucleic acids by a sequence of nonenzymatic glycation reactions, collectively known as the Maillard reaction [26,31]. Exogenous sources of AGE originate from diet [32] and tobacco smoking [33]. Endogenously, AGE formation is promoted by hyperglycemia, but also by high levels of oxidative stress [26].…”

Section: Uremic Inflammationmentioning

confidence: 99%

Inflammation and Premature Ageing in Chronic Kidney Disease

Ebert

Pawelzik

Witasp

et al. 2020

Toxins

162

122

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Persistent low-grade inflammation and premature ageing are hallmarks of the uremic phenotype and contribute to impaired health status, reduced quality of life, and premature mortality in chronic kidney disease (CKD). Because there is a huge global burden of disease due to CKD, treatment strategies targeting inflammation and premature ageing in CKD are of particular interest. Several distinct features of the uremic phenotype may represent potential treatment options to attenuate the risk of progression and poor outcome in CKD. The nuclear factor erythroid 2-related factor 2 (NRF2)–kelch-like erythroid cell-derived protein with CNC homology [ECH]-associated protein 1 (KEAP1) signaling pathway, the endocrine phosphate-fibroblast growth factor-23–klotho axis, increased cellular senescence, and impaired mitochondrial biogenesis are currently the most promising candidates, and different pharmaceutical compounds are already under evaluation. If studies in humans show beneficial effects, carefully phenotyped patients with CKD can benefit from them.

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Section: Uremic Inflammationmentioning

confidence: 99%

Inflammation and Premature Ageing in Chronic Kidney Disease

Ebert

Pawelzik

Witasp

et al. 2020

Toxins

162

122

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“…However, the effect of smoking on RAGE signaling is less well studied. It was shown that stimulation of gingival carcinoma epithelial cells with cigarette smoke extract (CSE) increases RAGE expression and the subsequent inflammatory reaction and induces oral squamous cell carcinoma cell invasion [6]. Furthermore, it was shown that RAGE knock-out mice had reduced cigarette smoke-induced neutrophilic airway inflammation [7].…”

Section: To the Editormentioning

confidence: 99%

AGER expression and alternative splicing in bronchial biopsies of smokers and never smokers

et al. 2019

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Cigarette smoking is one of the major risk factors for the development of chronic obstructive pulmonary disease (COPD). Evidence is accumulating that Receptor for Advanced Glycation-End products (RAGE)-signaling is a key pathway in the pathophysiology of COPD. To date, it is unknown how smoking affects RAGE expression. In the current study, we investigated the effect of smoking on AGER , the gene encoding RAGE, expression and on alternative splicing of AGER . To this end, we conducted RNA-Seq on bronchial biopsies for asymptomatic smokers ( n = 36) and never smokers ( n = 40). Total AGER gene expression was accessed using DESeq2, while alternative splicing was investigated by measuring the number of specific split reads spanning exon-exon junctions and the total split reads. One of the major isoforms of RAGE is endogenous soluble (es) RAGE, an anti-inflammatory decoy receptor, making up for approximately 10% of the total amount of soluble (s)RAGE. We found that smokers show decreased total gene expression of AGER in bronchial biopsies, while the relative abundance of the esRAGE isoform is increased. Furthermore, no difference in the serum levels of total sRAGE were observed between smokers and non-smokers. Our data indicates that smoking initiates a protective anti-inflammatory mechanism with decreased expression of the pro-inflammatory gene AGER and increased relative abundance of the anti-inflammatory isoform esRAGE.

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“…The RAGE is a pattern-recognition cell-surface receptor that experiences increased expression during exposure to tobacco smoke (Chapman et al, 2018;Robinson, Stogsdill, Lewis, Wood, & Reynolds, 2012;Winden et al, 2014). Expression of RAGE has been detected in gingival tissues from human subjects with chronic periodontitis and it is overexpressed in gingival tissues from smokers diagnosed with periodontal diseases (Chapman et al, 2018).…”

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confidence: 99%

Cell invasion, RAGE expression, and inflammation in oral squamous cell carcinoma (OSCC) cells exposed to e‐cigarette flavoring

Tsai

Budge

Lepre

et al. 2020

Clinical & Exp Dental Res

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Objective Electronic cigarettes have given rise to a new, largely unregulated market within the smoking industry. While generally supposed to be less harmful than traditional tobacco smoke, awareness of the biological effects of electronic cigarette liquid is still scarce. Our objective was to determine the impact of electronic cigarette flavoring and nicotine on gingival squamous cell carcinoma invasion, RAGE expression, and the elaboration of pro‐inflammatory molecules. Methods and Materials Gingival and tongue squamous cell carcinoma cells were exposed to Red Hot or Green Apple flavored electronic cigarette flavoring with or without nicotine. Immunofluorescence determined RAGE expression. Real‐time cellular invasion was assessed using a RTCA DP instrument. Culture medium was assayed for cytokine secretion. Results Compared to controls we observed: increased cell invasion in gingival cells with Red Hot electronic cigarette flavoring and decreased cell invasion with Green Apple; decreased cell invasion in tongue cells treated with Red Hot electronic cigarette flavoring and no differences in invasion with Green Apple; flavor and nicotine dependent increases in RAGE expression; and differential expression of IL‐1α, IL‐8, and MMP‐13. Conclusion We conclude that electronic cigarette flavoring and nicotine orchestrate differential regulation of oral squamous cell carcinoma (OSCC) cell invasion and inflammatory effects. This study provides an important initial step in dissecting RAGE‐mediated mechanisms of cancerous invasion and molecular avenues employed by OSCC.

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Cigarette smoke extract induces oral squamous cell carcinoma cell invasion in a receptor for advanced glycation end‐products‐dependent manner

Cited by 17 publications

References 42 publications

Inflammation and Premature Ageing in Chronic Kidney Disease

Inflammation and Premature Ageing in Chronic Kidney Disease

AGER expression and alternative splicing in bronchial biopsies of smokers and never smokers

Cell invasion, RAGE expression, and inflammation in oral squamous cell carcinoma (OSCC) cells exposed to e‐cigarette flavoring

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