Literature DB >> 31526129

The role of miR-130a-3p and SPOCK1 in tobacco exposed bronchial epithelial BEAS-2B transformed cells: Comparison to A549 and H1299 lung cancer cell lines.

Xiao-Fan Yu1,2, Jin Wang1,2, Nan OUYang1,2, Shuang Guo1, Huiying Sun1, Jian Tong1,2, Tao Chen1,2, Jianxiang Li1,2.   

Abstract

In the pathogenesis of human lung cancer induced by tobacco smoke decreased expression levels of microRNAs (miRNAs) are known to occur. At present, the specific miRNAs expression levels reduced by tobacco smoke and subsequent lung cellular transformation remain to be determined. The aim of this study was thus to identify the miRNAs affected following cigarette-smoke exposure in bronchial epithelial BEAS-2B cells that were malignantly transformed into S30 cells. In addition, the miRNAs in S30 transformed cells were compared to human lung cancer cell lines A549 and H1299. Our results identified miR-130a-3p which was down-regulated in S30 cells as well as A549 and H1299 lung cancer cell lines. Using miRNA mimic, a correlation between elevated miR-130a-3p expression levels and reduced migration in A549 and H1299 cell lines and S30 cells was noted as evidenced by transwell and wound healing assays accompanied by enhanced apoptosis. Further, two online target genes prediction programs TargetScan and miRDB were employed to identify the miRNA target gene SPOCK1 in all three cell types. SPOCK1 expression was higher in unexposed bronchial epithelial BEAS-2B cells. It is of interest that however silencing SPOCK1 in transformed S30 cells exposed to cigarette-smoke a marked depression in cell migration was noted. Our findings demonstrate that upregulated miR-130a-3p was associated with reduced SPOCK1 expression in transformed S30 as well as lung cancer A549 and H1299 cell lines indicating that cigarette transformed cells behave similar to lung cancer cells and this process involves diminished lung cancer cells migration.

Entities:  

Keywords:  Migration; SPOCK1; cigarette-smoke; lung cancer; miR-130a-3p

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Year:  2019        PMID: 31526129     DOI: 10.1080/15287394.2019.1664479

Source DB:  PubMed          Journal:  J Toxicol Environ Health A        ISSN: 0098-4108


  4 in total

1.  Protection of toll-like receptor 9 against lipopolysaccharide-induced inflammation and oxidative stress of pulmonary epithelial cells via MyD88-mediated pathways.

Authors:  Zhenhong Qi; Zhijie He; Jiaxin Chen; Mingyuan Ma; Menghua Deng; Yunhai Zhang; Tianwei Ma
Journal:  Physiol Res       Date:  2022-04-11       Impact factor: 2.139

2.  miR-130a-Mediated KLF3 Can Inhibit the Growth of Lung Cancer Cells.

Authors:  Ming-Chao Wei; Yu-Min Wang; Da-Wei Wang
Journal:  Cancer Manag Res       Date:  2021-04-06       Impact factor: 3.989

3.  MiR-130a-3p Alleviates Inflammatory and Fibrotic Phases of Pulmonary Fibrosis Through Proinflammatory Factor TNF-α and Profibrogenic Receptor TGF-βRII.

Authors:  Yan Ding; Yapeng Hou; Yanhong Liu; Tong Yu; Yong Cui; Hongguang Nie
Journal:  Front Pharmacol       Date:  2022-03-30       Impact factor: 5.810

Review 4.  SPOCK1 Involvement in Epithelial-to-Mesenchymal Transition: A New Target in Cancer Therapy?

Authors:  Li-Rui Sun; Si-Yu Li; Qiu-Shi Guo; Wei Zhou; Hong-Mei Zhang
Journal:  Cancer Manag Res       Date:  2020-05-18       Impact factor: 3.989

  4 in total

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