Evidence map›Paper›PMID 32795291›Full record

ArticleJournal of translational medicine2020

Identification and validation of smoking-related genes in lung adenocarcinoma using an in vitro carcinogenesis model and bioinformatics analysis.

Jin Wang, Tao Chen, Xiaofan Yu, Nan OUYang, Lirong Tan, Beibei Jia, Jian Tong, Jianxiang Li

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 26 citations in OpenAlex.

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  12. [Roles of Histidine Kinases and Histidine Phosphatases in Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2021
    Review
  13. Identification ofFrontiers in oncology · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Jin WangDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Renai Road, Suzhou, 215123, China.
Tao ChenDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Renai Road, Suzhou, 215123, China.
Xiaofan YuDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Renai Road, Suzhou, 215123, China.
Nan OUYangDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Renai Road, Suzhou, 215123, China.
Lirong TanDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Renai Road, Suzhou, 215123, China.
Beibei JiaDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Renai Road, Suzhou, 215123, China.
Jian TongDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Renai Road, Suzhou, 215123, China.
Jianxiang LiDepartment of Toxicology, School of Public Health, Medical College of Soochow University, Renai Road, Suzhou, 215123, China. aljxcr@suda.edu.cn.ORCID 0000-0001-6674-7703
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung cancer is one of the most common carcinomas in the world, and lung adenocarcinoma (LUAD) is the most lethal and most common subtype of lung cancer. Cigarette smoking is the most leading risk factor of lung cancer, but it is still unclear how normal lung cells become cancerous in cigarette smokers. This study aims to identify potential smoking-related biomarkers associated with the progression and prognosis of LUAD, as well as their regulation mechanism using an in vitro carcinogenesis model and bioinformatics analysis.

resultsBased on the integration analysis of four Gene Expression Omnibus (GEO) datasets and our mRNA sequencing analysis, 2 up-regulated and 11 down-regulated genes were identified in both S30 cells and LUAD. By analyzing the LUAD dataset in The Cancer Gene Analysis (TCGA) database, 3 of the 13 genes, viz., glycophorin C (GYPC), NME/NM23 nucleoside diphosphate kinase 1 (NME1) and slit guidance ligand 2 (SLIT2), were found to be significantly correlated with LUAD patients' smoking history. The expression levels of GYPC, NME1 and SLIT2 in S30 cells and lung cancer cell lines were validated by quantitative PCR, immunofluorescence, and western blot assays. Besides, these three genes are associated with tumor invasion depth, and elevated expression of NME1 was correlated with lymph node metastasis. The enrichment analysis suggested that these genes were highly correlated to tumorigenesis and metastasis-related biological processes and pathways. Moreover, the increased expression levels of GYPC and SLIT2, as well as decreased expression of NME1 were associated with a favorable prognosis in LUAD patients. Furthermore, based on the multi-omics data in the TCGA database, these genes were found to be regulated by DNA methylation.

conclusionIn conclusion, our observations indicated that the differential expression of GYPC, NME1 and SLIT2 may be regulated by DNA methylation, and they are associated with cigarette smoke-induced LUAD, as well as serve as prognostic factors in LUAD patients.

Indexed as

Adenocarcinoma of LungLung NeoplasmsCarcinogenesisComputational BiologyGene Expression Regulation, NeoplasticHumansSmokingCigarette smokeDNA methylationGYPCLung adenocarcinoma (LUAD)NME1prognosisSLIT2

Identifiers

PMID32795291
PMCPMC7427766
OpenAlexW3049262110

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.