Lung carcinogenesis by tobacco smoke

Hecht, Stephen S.

doi:10.1002/ijc.27816

Cited by 395 publications

(320 citation statements)

References 82 publications

(207 reference statements)

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“…Cigarette smoke remains to be a major etiological risk factor for lung cancer (1,4); a previous study reported that an increase in the incidence of LAC was correlated with cigarette smoking (5). In addition, several signaling pathway abnormalities in lung cancer have been found to be associated with smoking (6,7). Therefore, further studies that aim to identify the signals activated by smoking-associated carcinogens may aid in the development of targeted therapies for lung cancer patients with a history of smoking.…”

Section: Introductionmentioning

confidence: 99%

Cigarette smoke induces the expression of Notch3, not Notch1, protein in lung adenocarcinoma

Cheng

Tan

et al. 2015

Oncology Letters

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Abstract. The aim of the present study was to determine the effect of cigarette smoke on the expression of Notch proteins in lung adenocarcinoma (LAC). Protein expression levels of Notch1 and Notch3 were analyzed using immunohistochemistry in 102 human LAC specimens. Of these, 52 were obtained from smokers and 50 from non-smokers. In addition, cigarette smoke extract (CSE) at varying concentrations (1, 2.5 and 5%) was administered to A549 cells. The expression of Notch1 and Notch3 protein was then detected by western blot analysis at different time points (0, 8, 24 and 48 h). Of the 102 LAC specimens, 42 (41.2%) were positive for Notch1 and 63 (61.8%) were positive for Notch3. There was no significant difference in the level of Notch1 expression between smokers and non-smokers with LAC (P>0.05). The positive rate and staining intensity of Notch3 expression were increased in the smokers compared with the non-smokers (P<0.05). The expression of Notch3 protein in A549 cells increased in a time-and dose-dependent manner following treatment with CSE, whilst the expression of Notch1 protein appeared stable. The results suggested that cigarette smoke was able to induce the expression of Notch3, not Notch1, protein in LAC. The data revealed an upregulation of Notch3 in LAC following cigarette smoke exposure. Such findings may provide a novel therapeutic target for the treatment of LAC.

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Section: Introductionmentioning

confidence: 99%

Cigarette smoke induces the expression of Notch3, not Notch1, protein in lung adenocarcinoma

Cheng

Tan

et al. 2015

Oncology Letters

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“…10,11 The carcinogenesis for lung cancer by tobacco smoke derived significant attentions on B[a]P and NNK in lung cancer development and progression, inducing the mutations of Ras genes or P53 via different signal pathways. 12,13 For example, NNK-induced Kras mutation from…”

Section: Introductionmentioning

confidence: 99%

Benzopyrene promotes lung cancer A549 cell migration and invasion through up-regulating cytokine IL8 and chemokines CCL2 and CCL3 expression

Zhang

Jin

et al. 2016

Exp Biol Med (Maywood)

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Tobacco-sourced carcinogen including benzopyrene (B[a]P) in lung cancer metastasis has not been fully reported. In this study, lung carcinoma A549 cell line was used to investigate the potential roles of tobacco-sourced B[a]P on cell metastasis and invasion and to assess its underlying mechanism. Effects of tobacco-sourced carcinogen on A549 cell proliferation, metastasis, and invasion were analyzed using MTT assay, Transwell assay, and scratch method, respectively. The effects of tobacco-sourced carcinogen on cytokines and chemokines secretion were detected using enzyme-linked immunosorbent assay. Moreover, correlation between inflammatory factor expression and cancer cell migration and invasion was assessed using siRNA-mediated gene silencing. Data showed that both B[a]P and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone either at high or low dose performed no significant difference on A549 cell proliferation with time increasing. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone performed no significant difference on A549 cell migration and invasion while B[a]P significantly increased A549 cell migration and invasion compared to the control group (P < 0.05). Consequently, except for IL-6, IL-8, CCL-2, and CCL-3, secretions were significantly increased by B[a]P treatment compared to the control (P < 0.05). Furthermore, when CCL-2 and CCL-3 were silenced, the migrated and invasive A549 cells were significantly decreased compared to the control, respectively (P < 0.05), while silenced IL-8 drastically decreased the migrated and invasive cells compared to the control (P < 0.01). Taken together, this study illustrated that there may be significant correlation between smoking and lung cancer metastasis. B[a]P maybe an excellent contributor for lung cancer metastasis through up-regulating IL-8, CCL-2, and CCL-3 expression.

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“…Also found that cigarette smoking was the chief cause of death after notifying the symptoms of respiratory diseases, Trachea bronchus, pulmonary emphysema, oropharynx, and renal pelvis and for adenocarcinoma of the esophagus in smokers 16 .Smoke from cigarette contain plenty of carcinogenic chemicals, such as nicotine, CO, PAH and NNitrosamine etc. 17 .Principally, fifty five carcinogenic compounds, including amines, aldehydes, inorganic and organic compounds in smoke have tendency to nick bio molecules and DNA and may cause disorder in gene expression and cancer too 18 .The uncontrolled cell growth in lung tissues kills lung patients and pose a challenge for efforts to extend and improve the lives of these patients. The amount of functioning on all aspect of p53, reflects a key role in early event of lung carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%