Bioinformatics Analysis of the Effects of Tobacco Smoke on Gene Expression

Cao, Chunhua; Chen, Jianhua; Lyu, Chengqi; Yu, Jia; Zhao, Wei; Wang, Yi; Zou, Derong

doi:10.1371/journal.pone.0143377

Cited by 20 publications

(21 citation statements)

References 36 publications

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“…The dataset consists of 52 human samples; after excluding 4 samples that did not pass quality control, 26 normal kidney samples and 22 CKD samples were used to conduct DEGs analysis. DEGs were defined by the Bioconductor/R limma package as previously described [ 58 ]. Cut-off values of P < 0.01 and Fold Change |FC| ≥ 2 were applied.…”

Section: Methodsmentioning

confidence: 99%

NiaoDuQing granules relieve chronic kidney disease symptoms by decreasing renal fibrosis and anemia

Wang

Jia

et al. 2017

Oncotarget

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NiaoDuQing (NDQ) granules, a traditional Chinese medicine, has been clinically used in China for over fourteen years to treat chronic kidney disease (CKD). To elucidate the mechanisms underlying the therapeutic benefits of NDQ, we designed an approach incorporating chemoinformatics, bioinformatics, network biology methods, and cellular and molecular biology experiments. A total of 182 active compounds were identified in NDQ granules, and 397 putative targets associated with different diseases were derived through ADME modelling and target prediction tools. Protein-protein interaction networks of CKD-related and putative NDQ targets were constructed, and 219 candidate targets were identified based on topological features. Pathway enrichment analysis showed that the candidate targets were mostly related to the TGF-β, the p38MAPK, and the erythropoietin (EPO) receptor signaling pathways, which are known contributors to renal fibrosis and/or renal anemia. A rat model of CKD was established to validate the drug-target mechanisms predicted by the systems pharmacology analysis. Experimental results confirmed that NDQ granules exerted therapeutic effects on CKD and its comorbidities, including renal anemia, mainly by modulating the TGF-β and EPO signaling pathways. Thus, the pharmacological actions of NDQ on CKD symptoms correlated well with in silico predictions.

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Section: Methodsmentioning

confidence: 99%

NiaoDuQing granules relieve chronic kidney disease symptoms by decreasing renal fibrosis and anemia

Wang

Jia

et al. 2017

Oncotarget

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“…In addition to human malignancies, there was a clear increase in CYP1B1 promoter CpG island methylation level in isoniazid-induced liver injury in rats (Li et al, 2018). Interestingly, bioinformatics analyses by Cao et al identified CYP1B1 as a potential target in smoking-mediating malignancies (Cao et al, 2015). Experimental analysis further demonstrated that hypo-methylated CYP1B1 was up-regulated in current smokers (Tsai et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Overexpression of MECP2 attenuates cigarette smoke extracts induced lung epithelial cell injury by promoting CYP1B1 methylation

et al. 2020

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MECP2 (Methyl-CpG-binding protein 2) has been shown to have a critical role in regulating DNA methylation against smoke exposed lung injury. However, the biological function of MECP2 and the underlying molecular mechanism remains elusive. Human bronchial epithelial (16HBE) and alveolar type II epithelial cells (AECII) were exposed to increasing concentrations of cigarette smoke extracts (CSE) solution to establish CSE-induced lung epithelial cell injury models. Our findings revealed that MECP2 was down-regulated, while CYP1B1 was up-regulated in CSE-induced lung epithelial cell injury models by quantitative real time PCR, western blotting and immunofluorescence staining. Down-regulated CYP1B1 was ascribed to the demethylation of its promoter by methylation-specific PCR (MSP). The in vitro experiments further showed that MECP2 overexpression significantly attenuated CSE-triggered cell growth attenuation, cell cycle arrest, apoptosis and ROS generation in lung epithelial cells by CCK-8 and flow cytometry assays. In molecular level, we further demonstrated that MECP2 overexpression obviously suppressed the expression of CYP1B1 through enhancing DNA methylation. Therefore, our data suggest that MECP2 protects against CSE-induced lung epithelial cell injury possibly through down-regulating CYP1B1 expression via elevating its methylation status.

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“…In contrast to studies assessing lung cancer via bioinformatics tools 15 – 19 , a few studies have focused on smoking with a systems biology approach; for instance, expression-based network analysis and assessment of protein-protein interactions have revealed changes in human blood 20 , human buccal mucosa 21 , and mouse lung samples 22 due to cigarette exposure. For exhibiting the direct correlation between smoking and lung cancer, Ying Liu et al .…”

Section: Introductionmentioning

confidence: 99%

Comparative Network Analysis of Patients with Non-Small Cell Lung Cancer and Smokers for Representing Potential Therapeutic Targets

Pazhouhandeh

Samiee

Boniadi

et al. 2017

Sci Rep

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Cigarette smoking is the leading cause of lung cancer worldwide. In this study, we evaluated the serum autoantibody (AAb) repertoires of non-small cell lung cancer (NSCLC) patients and smokers (SM), leading to the identification of overactivated pathways and hubs involved in the pathogenesis of NSCLC. Surface- and solution-phase biopanning were performed on immunoglobulin G purified from the sera of NSCLC and SM groups. In total, 20 NSCLC- and 12 SM-specific peptides were detected, which were used to generate NSCLC and SM protein datasets. NSCLC- and SM-related proteins were visualized using STRING and Gephi, and their modules were analyzed using Enrichr. By integrating the overrepresented pathways such as pathways in cancer, epithelial growth factor receptor, c-Met, interleukin-4 (IL-4) and IL-6 signaling pathways, along with a set of proteins (e.g. phospholipase D (PLD), IL-4 receptor, IL-17 receptor, laminins, collagens, and mucins) into the PLD pathway and inflammatory cytokines network as the most critical events in both groups, two super networks were made to elucidate new aspects of NSCLC pathogenesis and to determine the influence of cigarette smoking on tumour formation. Taken together, assessment of the AAb repertoires using a systems biology approach can delineate the hidden events involved in various disorders.

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Bioinformatics Analysis of the Effects of Tobacco Smoke on Gene Expression

Cited by 20 publications

References 36 publications

NiaoDuQing granules relieve chronic kidney disease symptoms by decreasing renal fibrosis and anemia

NiaoDuQing granules relieve chronic kidney disease symptoms by decreasing renal fibrosis and anemia

Overexpression of MECP2 attenuates cigarette smoke extracts induced lung epithelial cell injury by promoting CYP1B1 methylation

Comparative Network Analysis of Patients with Non-Small Cell Lung Cancer and Smokers for Representing Potential Therapeutic Targets

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