scholarly journals Prenatal N-acetylcysteine prevents cigarette smoke-induced lung cancer in neonatal mice

2009 ◽  
Vol 30 (8) ◽  
pp. 1398-1401 ◽  
Author(s):  
R. Balansky ◽  
G. Ganchev ◽  
M. Iltcheva ◽  
V. E. Steele ◽  
S. De Flora
Keyword(s):  
Lung Cancer ◽  
Cigarette Smoke ◽  
Neonatal Mice

Cigarette smoke extract reduces FOXO3a promoting tumor progression and cell migration in lung cancer

Toxicology ◽  
2021 ◽  
pp. 152751
Author(s):  
Serena Di Vincenzo ◽  
Claudia Sangiorgi ◽  
Maria Ferraro ◽  
Marco Buscetta ◽  
Chiara Cipollina ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Migration ◽  
Tumor Progression ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract

scholarly journals Gene expression profiling of epigenetic chromatin modification enzymes and histone marks by cigarette smoke: implications for COPD and lung cancer

2016 ◽  
Vol 311 (6) ◽  
pp. L1245-L1258 ◽  
Author(s):  
Isaac K. Sundar ◽  
Irfan Rahman
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Dna Methylation ◽  
Cigarette Smoke ◽  
Histone Modifications ◽  
Expression Patterns ◽  
Chromatin Modification ◽  
Gene Expression Patterns ◽  
Validation Data ◽  
Histone Marks

Chromatin-modifying enzymes mediate DNA methylation and histone modifications on recruitment to specific target gene loci in response to various stimuli. The key enzymes that regulate chromatin accessibility for maintenance of modifications in DNA and histones, and for modulation of gene expression patterns in response to cigarette smoke (CS), are not known. We hypothesize that CS exposure alters the gene expression patterns of chromatin-modifying enzymes, which then affects multiple downstream pathways involved in the response to CS. We have, therefore, analyzed chromatin-modifying enzyme profiles and validated by quantitative real-time PCR (qPCR). We also performed immunoblot analysis of targeted histone marks in C57BL/6J mice exposed to acute and subchronic CS, and of lungs from nonsmokers, smokers, and patients with chronic obstructive pulmonary disease (COPD). We found a significant increase in expression of several chromatin modification enzymes, including DNA methyltransferases, histone acetyltransferases, histone methyltransferases, and SET domain proteins, histone kinases, and ubiquitinases. Our qPCR validation data revealed a significant downregulation of Dnmt1, Dnmt3a, Dnmt3b, Hdac2, Hdac4, Hat1, Prmt1, and Aurkb. We identified targeted chromatin histone marks (H3K56ac and H4K12ac), which are induced by CS. Thus CS-induced genotoxic stress differentially affects the expression of epigenetic modulators that regulate transcription of target genes via DNA methylation and site-specific histone modifications. This may have implications in devising epigenetic-based therapies for COPD and lung cancer.

Cigarette smoke and increased COX-2 and survivin levels in exhaled breath condensate of lung cancer patients: How hot is the link?

Lung Cancer ◽  
2010 ◽  
Vol 67 (1) ◽  
pp. 108-113 ◽  
Author(s):  
Giovanna E. Carpagnano ◽  
Antonio Spanevello ◽  
Grazia P. Palladino ◽  
Claudia Gramiccioni ◽  
Cinzia Ruggieri ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Cigarette Smoke ◽  
Exhaled Breath Condensate ◽  
Exhaled Breath ◽  
Lung Cancer Patients ◽  
Cox 2 ◽  
Breath Condensate

scholarly journals FERMT3 mediates cigarette smoke-induced epithelial–mesenchymal transition through Wnt/β-catenin signaling

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Xiaoshan Su ◽  
Junjie Chen ◽  
Xiaoping Lin ◽  
Xiaoyang Chen ◽  
Zhixing Zhu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Migration ◽  
Cigarette Smoke ◽  
Epithelial Mesenchymal Transition ◽  
Control Group ◽  
Data Set ◽  
Mesenchymal Transition

Abstract Background Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease (COPD) and lung cancer. Epithelial–mesenchymal transition (EMT) is an essential pathophysiological process in COPD and plays an important role in airway remodeling, fibrosis, and malignant transformation of COPD. Previous studies have indicated FERMT3 is downregulated and plays a tumor-suppressive role in lung cancer. However, the role of FERMT3 in COPD, including EMT, has not yet been investigated. Methods The present study aimed to explore the potential role of FERMT3 in COPD and its underlying molecular mechanisms. Three GEO datasets were utilized to analyse FERMT3 gene expression profiles in COPD. We then established EMT animal models and cell models through cigarette smoke (CS) or cigarette smoke extract (CSE) exposure to detect the expression of FERMT3 and EMT markers. RT-PCR, western blot, immunohistochemical, cell migration, and cell cycle were employed to investigate the potential regulatory effect of FERMT3 in CSE-induced EMT. Results Based on Gene Expression Omnibus (GEO) data set analysis, FERMT3 expression in bronchoalveolar lavage fluid was lower in COPD smokers than in non-smokers or smokers. Moreover, FERMT3 expression was significantly down-regulated in lung tissues of COPD GOLD 4 patients compared with the control group. Cigarette smoke exposure reduced the FERMT3 expression and induces EMT both in vivo and in vitro. The results showed that overexpression of FERMT3 could inhibit EMT induced by CSE in A549 cells. Furthermore, the CSE-induced cell migration and cell cycle progression were reversed by FERMT3 overexpression. Mechanistically, our study showed that overexpression of FERMT3 inhibited CSE-induced EMT through the Wnt/β-catenin signaling. Conclusions In summary, these data suggest FERMT3 regulates cigarette smoke-induced epithelial–mesenchymal transition through Wnt/β-catenin signaling. These findings indicated that FERMT3 was correlated with the development of COPD and may serve as a potential target for both COPD and lung cancer.

scholarly journals Smart Air Filter Based on Activated Charcoal and Aloe Vera Using Fuzzy Logic Algorithm

2021 ◽  
Vol 2111 (1) ◽  
pp. 012047
Author(s):  
F Arifin ◽  
W R Gusti ◽  
A Nasuha ◽  
A S Priambodo ◽  
A Winursito
Keyword(s):  
Lung Cancer ◽  
Fuzzy Logic ◽  
Cigarette Smoke ◽  
Activated Charcoal ◽  
Control Method ◽  
Aloe Vera ◽  
Smart Device ◽  
Upper Respiratory Tract ◽  
Fuzzy Logic Algorithm ◽  
Tract Cancer

Abstract Smoking is one of the main risk factors of several chronic diseases such as lung cancer, upper respiratory tract cancer, heart disease, stroke, bronchitis, emphysema and others, even smoking can cause death. Cigarette smoke inhaled by passive smoking is the main cause of lung cancer in people who are not smokers. The risk of lung cancer increases by 20-30% in non-smokers but always surrounded by cigarette smoke, compared to non-smokers who are not exposed to smoke. This study aims to develop a smart device to filter cigarette smoke so that the air released from this device is free from the dangers of cigarette smoke. The materials used in this device as a cigarette smoke filter are activated charcoal and aloe vera, the pores of the charcoal open and can become adsorbents. This device uses fuzzy logic as a control method that can provide decisions that resemble human decisions. Arduino is used to adjust the fan rotation in absorb cigarette smoke and the LCD to display the level of cigarette smoke.

scholarly journals miRNA and proteomic dysregulation in non-small cell lung cancer in response to cigarette smoke

2017 ◽  
Vol 1 (Special Issue-Supplement) ◽  
pp. 244-244
Author(s):  
Niraj Babu ◽  
Jayshree Advani ◽  
Hitendra S. Solanki ◽  
Krishna Patel ◽  
Ankit Jain ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cigarette Smoke ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung

A Review of the Histopathology of Cigarette Smoke–Induced Lung Cancer in Rats and Mice

2007 ◽  
Vol 26 (4) ◽  
pp. 307-313 ◽  
Author(s):  
Fletcher F. Hahn ◽  
Andrew P. Gigliotti ◽  
Julie A. Hutt ◽  
Thomas H. March ◽  
Joe L. Mauderly
Keyword(s):  
Lung Cancer ◽  
Cigarette Smoke ◽  
Malignant Tumors ◽  
Lung Tumors ◽  
The Past ◽  
Lifetime Exposure ◽  
Low Incidence ◽  
Epithelial Lesions ◽  
Induced Changes ◽  
Rats And Mice

In the past several years an increased number of lung tumors has been reported in laboratory studies of rats and mice after lifetime exposure to mainstream cigarette smoke. Proliferative epithelial lesions are present in the lungs of both species and are apparent antecedent lesions to benign and malignant tumors. Both species have alveolar epithelia hyperplasia, alveolar adenomas, and alveolar carcinomas. The incidence of all three are more in the rats. In addition, mice also have bronchiolar epithelial hyperplasia and bronchial papillomas not found in rats. Rats have a low incidence of squamous cyst that is not found in mice. Lung tumors in rats and mice are found at the end of the life span and rarely metastasize. The characteristics of the lung tumors, and the proliferative changes associated with the tumors, are important in helping understand the mechanisms of lung cancer induction. These studies in rats and mice allow new approaches to the study of cigarette smoke–induced changes in the lung.

Cigarette Smoke-Induced Reduction of 14-3-3σ Expression Promotes The Progression of Non-Small Cell Lung Cancer

2021 ◽  
Author(s):  
Longxia Dai ◽  
Quanwen Deng ◽  
Aibin Liu ◽  
Shuya He ◽  
Qiong Chen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Expression ◽  
Small Cell Lung Cancer ◽  
Cigarette Smoke ◽  
Cell Lung Cancer ◽  
A549 Cells ◽  
Small Cell ◽  
Small Cell Lung ◽  
Smoking Group ◽  
The Relationship

Abstract Background Lung cancer is a common malignant tumour and the leading cause of cancer death. Smoking is closely related to lung cancer, which can not only induce the occurrence of lung cancer but also affect its progress and prognosis. Objectives To investigated the relationship between smoking and 14-3-3σ protein expression in non-small-cell lung cancer (NSCLC), investigated the relationship between 14-3-3σ expression and cell migration in A549 cells induced by cigarette smoke extract (CSE) and explored whether DNA methylation plays a role in the decreased expression of 14-3-3σ induced by CSE. Methods 14-3-3σ protein expression was examined by immunohistochemistry in 152 NSCLC tissue samples. In vitro experiments were divided into three groups: The current smoking group (CS), the ex-smoking group (ES) and the normal control group (NC). Cell transfection was used for 14-3-3σ protein overexpression. The mRNA and protein expression levels of 14-3-3σ were detected by RT-PCR and Western blotting, respectively. Cell migration was detected by Transwell and wound-healing assays, and the methylation of 14-3-3σ was detected by methylation-specific PCR. Results 14-3-3σ protein expression was decreased in NSCLC patients with a history of smoking. The expression of 14-3-3σ was decreased in A549 cells treated with CSE. The migration capacity of A549 cells treated with CSE was enhanced. DNA methylation in the cigarette smoke-treated A549 cells was higher than that in the untreated cells. Conclusion Cigarette smoke induced reduction of 14-3-3σ expression can promote the progression of non-small cell lung cancer.

scholarly journals Cigarette smoke affects the onco-suppressor DAB2IP expression in bronchial epithelial cells of COPD patients

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Giulia Anzalone ◽  
Giuseppe Arcoleo ◽  
Fabio Bucchieri ◽  
Angela M. Montalbano ◽  
Roberto Marchese ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Mesenchymal Transition ◽  
Copd Patients ◽  
Ezh2 Expression

Abstract Cigarette smoke is a risk factor for COPD and lung cancer. In cancer, epigenetic modifications affect the expression of Enhancer of Zester Homolog 2 (EZH2), and silenced disabled homolog 2 interacting protein gene (DAB2IP) (onco-suppressor gene) by Histone H3 tri-methylation in lysine 27 (H3K27me3). In“ex vivo”studies, we assessed EZH2, H3K27me3 and DAB2IP immunoreactivity in bronchial epithelial cells from COPD patients (smokers, ex-smokers), Smoker and control subjects. In“in vitro” experiments we studied the effect of cigarette smoke extract (CSE) on EZH2/H3K27me3/DAB2IP expression, apoptosis, invasiveness, and vimentin expression in 16HBE, primary cells, and lung cancer cell lines (A549) long-term exposed to CSE. Finally, in “in vitro”studies, we tested the effect of GSK343 (selective inhibitor of EZH2). EZH2 and H3K27me3 expression was higher, while DAB2IP was lower levels, in bronchial epithelium from COPD and Smokers than in Controls. CSE increased EZH2, H3K27me3 expression and decreased DAB2IP, cell apoptosis and invasiveness in epithelial cells. GSK343 restored the effects of CSE. Cigarette smoke affects EZH2 expression, and reduced DAB2IP via H3K27me3 in COPD patients. The molecular mechanisms associated with EZH2 expression, generate a dysregulation of cell apoptosis, mesenchymal transition, and cell invasiveness in bronchial epithelial cells, encouraging the progression of airway inflammation toward lung cancer in COPD patients.

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