Dataset Information

Persistence of smoking induced non-small cell lung carcinogenesis by decreasing ERBB pathway-related microRNA expression.

ABSTRACT:

Background

Tobacco use is responsible for approximately 80-90% of non-small cell lung cancer cases. A large evidence base has shown that the ERBB pathway is associated with the occurrence of lung cancer. However, the mechanisms of how smoking activates the ERBB pathway have yet to be explained. We hypothesized that microRNAs may induce ERBB pathway activity during the process of lung cancer carcinogenesis.

Methods

We analyzed microRNA array data from the Gene Expression Omnibus and the Kyoto Encyclopedia of Genes and Genomes to determine any associations between genes and smoking in three groups of patients with NSCLC: smokers, former smokers, and non-smokers.

Results

The interaction network among miRNAs, including hsa-mir-185-3p, hsa-mir-4295, hsa-mir-4288, and hsa-mir-613, promotes lung cancer development by affecting the ERBB pathway.

Conclusion

Our findings provide evidence to explain the mechanism of lung cancer development in smokers.

SUBMITTER: Zhang L

PROVIDER: S-EPMC6449224 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Publications

Persistence of smoking induced non-small cell lung carcinogenesis by decreasing ERBB pathway-related microRNA expression.

Zhang Lianmin L Wang Hailong H Wang Changli C

Thoracic cancer 20190313 4

<h4>Background</h4>Tobacco use is responsible for approximately 80-90% of non-small cell lung cancer cases. A large evidence base has shown that the ERBB pathway is associated with the occurrence of lung cancer. However, the mechanisms of how smoking activates the ERBB pathway have yet to be explained. We hypothesized that microRNAs may induce ERBB pathway activity during the process of lung cancer carcinogenesis.<h4>Methods</h4>We analyzed microRNA array data from the Gene Expression Omnibus an ...[more]

PMID: 30868748

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Project description: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.

Dataset Information

Persistence of smoking induced non-small cell lung carcinogenesis by decreasing ERBB pathway-related microRNA expression.

Background

Methods

Results

Conclusion

Publications

Persistence of smoking induced non-small cell lung carcinogenesis by decreasing ERBB pathway-related microRNA expression.

Similar Datasets

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