Effects of Smoking Cessation on Gene Expression in Human Leukocytes of Chronic Smoker

Kim, Soo-Jeong; Kim, Su Young; Kim, Jae Hwa; Kim, Daijin

doi:10.4306/pi.2014.11.3.290

Cited by 4 publications

(1 citation statement)

References 40 publications

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“…MAPK3 is a kinase that has various biological functions, including promoting cell growth, cell proliferation, and cell cycle progression in a variety of cancers. [22][23][24][25] MOV10 is regarded as an important regulator of the nervous system, which promotes angiogenesis of glioma cells by regulating cell activity, migration, and tube formation. 26 Abnormal expression of MOV10 is related to radiotherapy resistance and cell proliferation in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

BCAR1 promotes proliferation and cell growth in lung adenocarcinoma via upregulation of POLR2A

et al. 2020

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Background This study was designed to investigate the effects of a novel carcinogenetic molecule, p130cas (breast cancer antiestrogen resistance protein 1 or BCAR1) on proliferation and cell growth in lung adenocarcinoma. The study also aimed to identify the possible underlying signal networks of BCAR1. Methods First, we evaluated proliferation, cell colony formation, apoptosis, and cell cycle after BCAR1 was knocked out (KO) using CRISPR‐Cas9 technology in H1975 and H1299 human lung adenocarcinoma cells. Subsequently, BCAR1 was upregulated in 293T cells and immunoprecipitation‐mass spectrometry (IP‐MS) was used with bioinformatics analysis to screen for potential networks of BCAR1 interacting proteins. Ultimately, we validated the correlated expressions of BCAR1 and a selected hub gene, RNA polymerase II subunit A (POLR2A), in 54 lung adenocarcinoma tissues, as well as in H1975 and H1299 cells. Results Cell proliferation of H1975 and H1299 was significantly inhibited following BCAR1‐KO. Colony formation of H1975 cells was also significantly decreased following BCAR1‐KO. IP‐MS demonstrated 419 potential proteins that may interact with BCAR1. Among them, 68 genes were significantly positively correlated to BCAR1 expression, as verified by TCGA. Six hub genes were revealed by PPI String. High expression of POLR2A, MAPK3, MOV10, and XAB2 predicted poor prognosis in lung adenocarcinoma, as verified by the K‐M plotter database. POLR2A and MAPK3 are involved in both catalytic activity and transferase activity. POLR2A and BCAR1 were significantly increased in lung cancer tissues as compared with matched normal tissues. High expression of POLR2A was significantly positively correlated to BCAR1 overexpression and predicted poor prognosis in 54 lung cancer cases. POLR2A expression was significantly decreased following BCAR1‐KO in H1975 and H1299 cells. Conclusions BCAR1 promotes proliferation and cell growth, probably via upregulation of POLR2A and subsequent enhancement of catalytic and transferase activities. However, additional robust studies are required to elucidate the mechanisms involved.

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Section: Discussionmentioning

confidence: 99%

BCAR1 promotes proliferation and cell growth in lung adenocarcinoma via upregulation of POLR2A

et al. 2020

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Evaluating the interaction between 3'aQTL and alcohol consumption/smoking on anxiety and depression: 3'aQTL-by-environment interaction study in UK Biobank cohort

Yang

Cheng

et al. 2023

Journal of Affective Disorders

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Effect of smoking on gene expression profile – overall mechanism, impact on respiratory system function, and reference to electronic cigarettes

Kopa

Pawliczak

2018

Toxicology Mechanisms and Methods

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Cigarette smoke has a crucial impact on transcriptome alteration by its effect on chromatin remodeling and DNA methylation status. The first mechanism is associated with the histone acetylation/deacetylation balance damage as a result of increased activity of NFĸB and lipid peroxidation products, which lead to an increased activity of HATs and DNMTs and reduced HDACs. The second mechanism is connected with direct damaging of DNA by smoke components, activation of downstream repair mechanism and recruitment of DNMTs into the breakage site, 'nicotine effect' and carbon monoxide (CO) activity on gene transcription and DNA methylation reduction. Cigarette smoking activates oxidative and inflammatory response and leads to uncontrolled structural changes in airways and alters gene expression. Such changes have a characteristic similar to that for COPD patients. Therefore, smoking is determined as a key risk factor for chronic respiratory disease development. Furthermore, electronic cigarettes, an alternative of tobacco cigarettes, also affect gene expression profile, which suggests some similarities in action mechanisms for both conventional and electronic cigarettes. However, there is only a limited number of trials discussing this issue and future investigations are needed.

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Effects of Smoking Cessation on Gene Expression in Human Leukocytes of Chronic Smoker

Cited by 4 publications

References 40 publications

BCAR1 promotes proliferation and cell growth in lung adenocarcinoma via upregulation of POLR2A

BCAR1 promotes proliferation and cell growth in lung adenocarcinoma via upregulation of POLR2A

Evaluating the interaction between 3'aQTL and alcohol consumption/smoking on anxiety and depression: 3'aQTL-by-environment interaction study in UK Biobank cohort

Effect of smoking on gene expression profile – overall mechanism, impact on respiratory system function, and reference to electronic cigarettes

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