scholarly journals MicroRNA profiling in BEAS-2B cells exposed to alpha radiation reveals potential biomarkers for malignant cellular transformation

2020 ◽  
Vol 9 (6) ◽  
pp. 834-844
Author(s):  
Xuhong Dang ◽  
Haipeng Lin ◽  
Youchen Li ◽  
Xiuli Guo ◽  
Yayi Yuan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Epithelial Cells ◽  
Alpha Particle ◽  
Cell Transformation ◽  
Malignant Cell ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Radon Exposure ◽  
Particle Irradiation ◽  
Malignant Cell Transformation

Abstract The carcinogenicity of radon has been convincingly documented through epidemiological studies of underground miners. The risk of lung cancer from radon exposure is due to the continuous radioactive decay of this gas and subsequent emission of high-energy alpha decay particles. And the bronchial epithelial cells are the main targets of radon exposure. However, there is a lack of early warning indicators of lung cancer caused by radon in the physical examination of populations involved in occupations with higher exposure to radon. To assess the potential of a molecular-based marker approach for the early detection of human lung cancer induced by radon, human bronchial epithelial cell injury models induced by alpha-particle irradiation were constructed. The results of transwell migration assay, transwell invasion assay, and the expression of the epithelial–mesenchymal transition-related proteins showed that malignant cell transformation could be triggered by alpha irradiation. Potential microRNAs (miRNAs) (hsa-miR-3907, hsa-miR-6732-3p, hsa-miR-4788, hsa-miR-5001-5p, and hsa-miR-4257) were screened using miRNA chips in cell models. The pathway analyses of miRNAs selected using DIANA-miRPath v3.0 showed that miRNAs involved in malignant cell transformation were associated with cell adhesion molecules, extracellular matrix receptor interaction, and proteoglycans in cancer, among others, which are closely related to the occurrence and development of carcinogenesis. Reverse Transcription Quantitative Real-Time PCR (RT-qPCR) assay showed that five screened miRNAs were up-regulated in five lung cancer tissue samples. In conclusion, the results indicated that hsa-miR-3907, hsa-miR-6732-3p, hsa-miR-4788, hsa-miR-5001-5p, and hsa-miR-4257 may be potential early markers of the malignant transformation of bronchial epithelial cells induced by alpha-particle irradiation.

Tobacco Smoking: Risk to Develop Addiction, Chronic Obstructive Pulmonary Disease, and Lung Cancer

2019 ◽  
Vol 14 (1) ◽  
pp. 39-52 ◽  
Author(s):  
Alessia Santoro ◽  
Carlo Tomino ◽  
Giulia Prinzi ◽  
Palma Lamonaca ◽  
Vittorio Cardaci ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Chronic Obstructive Pulmonary Disease ◽  
Epithelial Cells ◽  
Pulmonary Disease ◽  
Tobacco Smoking ◽  
Nicotinic Receptors ◽  
Bronchial Epithelial Cells ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Bronchial Epithelial

Background: The morbidity and mortality associated with tobacco smoking is well established. Nicotine is the addictive component of tobacco. Nicotine, through the non-neuronal α7nicotinic receptor, induces cell proliferation, neo-angiogenesis, epithelial to mesenchymal transition, and inhibits drug-induced apoptosis. Objective: To understand the genetic, molecular and cellular biology of addiction, chronic obstructive pulmonary disease and lung cancer. Methods: The search for papers to be included in the review was performed during the months of July- September 2018 in the following databases: PubMed (http://www.ncbi.nlm.nih.gov), Scopus (http://www.scopus.com), EMBASE (http://www.elsevier.com/online-tools/embase), and ISI Web of Knowledge (http://apps.webofknowledge.com/). The following searching terms: “nicotine”, “nicotinic receptor”, and “addiction” or “COPD” or “lung cancer” were used. </P><P> Patents were retrieved in clinicaltrials.gov (https://clinicaltrials.gov/). All papers written in English were evaluated. The reference list of retrieved articles was also reviewed to identify other eligible studies that were not indexed by the above-mentioned databases. </P><P> New experimental data on the ability of nicotine to promote transformation of human bronchial epithelial cells, exposed for one hour to Benzo[a]pyrene-7,8-diol-9-10-epoxide, are reported. Results: Nicotinic receptors variants and nicotinic receptors upregulation are involved in addiction, chronic obstructive pulmonary disease and/or lung cancer. Nicotine through α7nicotinic receptor upregulation induces complete bronchial epithelial cells transformation. Conclusion: Genetic studies highlight the involvement of nicotinic receptors variants in addiction, chronic obstructive pulmonary disease and/or lung cancer. A future important step will be to translate these genetic findings to clinical practice. Interventions able to help smoking cessation in nicotine dependence subjects, under patent, are reported.

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.

728 Loss of chromosome 9q21-23 in nonmalignant bronchial epithelial cells from individuals at risk for lung cancer

Lung Cancer ◽  
1997 ◽  
Vol 18 ◽  
pp. 187
Author(s):  
S. Belinsky ◽  
R. Crowell ◽  
R. Neft ◽  
F. Gilliland ◽  
J. Lechner
Keyword(s):  
Lung Cancer ◽  
At Risk ◽  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial

Cigarette smoke alters the EZH2/DAB2IP expression in bronchial epithelial cells. A risk factor for lung cancer in COPD patients

2016 ◽  
Author(s):  
Giulia Anzalone ◽  
Giuseppe Arcoleo ◽  
Angela Marina Montalbano ◽  
Rosalia Gagliardo ◽  
Fabio Bucchieri ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Risk Factor ◽  
Epithelial Cells ◽  
Cigarette Smoke ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Copd Patients

scholarly journals Aberrations of chromosome 19 in asbestos-associated lung cancer and in asbestos-induced micronuclei of bronchial epithelial cells in vitro

2008 ◽  
Vol 29 (5) ◽  
pp. 913-917 ◽  
Author(s):  
Salla T. Ruosaari ◽  
Penny E.H. Nymark ◽  
Mervi M. Aavikko ◽  
Eeva Kettunen ◽  
Sakari Knuutila ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Chromosome 19 ◽  
Bronchial Epithelial

scholarly journals Haplotype and diplotype analyses of variation in ERCC5 transcription cis-regulation in normal bronchial epithelial cells

2016 ◽  
Vol 48 (7) ◽  
pp. 537-543 ◽  
Author(s):  
Xiaolu Zhang ◽  
Erin L. Crawford ◽  
Thomas M. Blomquist ◽  
Sadik A. Khuder ◽  
Jiyoun Yeo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Epithelial Cells ◽  
Cancer Risk ◽  
Lung Cancer Risk ◽  
Excision Repair ◽  
Transcript Abundance ◽  
Bronchial Epithelial Cells ◽  
Interindividual Variation ◽  
Bronchial Epithelial ◽  
Allele Specific

Excision repair cross-complementation group 5 ( ERCC5) gene plays an important role in nucleotide excision repair, and dysregulation of ERCC5 is associated with increased lung cancer risk. Haplotype and diplotype analyses were conducted in normal bronchial epithelial cells (NBEC) to better understand mechanisms responsible for interindividual variation in transcript abundance regulation of ERCC5. We determined genotypes at putative ERCC5 cis-regulatory SNPs ( cis-rSNP) rs751402 and rs2296147, and marker SNPs rs1047768 and rs17655. ERCC5 allele-specific transcript abundance was assessed by a recently developed targeted sequencing method. Syntenic relationships among alleles at rs751402, rs2296147, and rs1047768 were assessed by allele-specific PCR followed by Sanger sequencing. We then assessed association of ERCC5 allele-specific expression at rs1047768 with haplotype and diplotype structure at cis-rSNPs rs751402 and rs2296147. Genotype analysis revealed significantly ( P < 0.005) higher interindividual variation in allelic ratios in cDNA samples relative to matched gDNA samples at both rs1047768 and rs17655. By diplotype analysis, mean expression was higher at the rs1047768 alleles syntenic with rs2296147 T allele compared with rs2296147 C allele. Furthermore, mean expression was lower at rs17655 C allele, which is syntenic with G allele at a linked SNP rs873601 ( D′ = 0.95). These data support the conclusions that in NBEC, T allele at SNP rs2296147 upregulates ERCC5, variation at rs751402 does not alter ERCC5 regulation, and that C allele at SNP rs17655 downregulates ERCC5. Variation in ERCC5 transcript abundance associated with allelic variation at these SNPs could result in variation in NER function in NBEC and lung cancer risk.

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