miR‑200b upregulation promotes migration of BEAS‑2B cells following long‑term exposure to cigarette smoke by targeting ETS1
Autor: | Beibei Jia, Jin Wang, Lirong Tan, Nan Ouyang, Jian Tong, Ruixin Yao, Qiulin Luo, Yezhou Li, Jianxiang Li |
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Rok vydání: | 2021 |
Předmět: |
Cancer Research
Epithelial-Mesenchymal Transition Lung Neoplasms Time Factors Cell Adenocarcinoma of Lung Biology migration Biochemistry Cell Line Proto-Oncogene Protein c-ets-1 Downregulation and upregulation ETS1 Antigens CD Cell Movement Tobacco Genetics medicine Humans Molecular Biology Gene knockdown Migration Assay Oncogene cigarette smoke Smoking Epithelial Cells Articles microRNA-200b Cell cycle Cadherins Up-Regulation Gene Expression Regulation Neoplastic MicroRNAs lung cancer medicine.anatomical_structure Oncology Cancer research Carcinoma Squamous Cell Molecular Medicine Wound healing |
Zdroj: | Molecular Medicine Reports |
ISSN: | 1791-3004 |
Popis: | Cigarette smoking is the leading cause of all histological types of lung cancer, and the role that microRNAs (miRNAs) serve in its pathogenesis is being increasingly recognized. The aim of the present study was to investigate the role of miR‑200b on migration in cigarette smoke‑induced malignant transformed cells. In the present study, miR‑200b expression was found to be increased in cigarette smoke (CS)‑exposed BEAS‑2B cells, lung cancer cell lines and tumor tissue samples. Using wound healing and Transwell migration assays, the migratory ability was shown to be increased in miR‑200b‑overexpressing cells, whereas miR‑200b knockdown resulted in reduced migration. Additionally, the expression of E‑Cadherin was downregulated, whereas that of N‑Cadherin was upregulated in miR‑200b mimic‑transfected cells, suggesting an increase in epithelial‑mesenchymal transition. Downstream, using four target gene prediction tools, six target genes of miR‑200b were predicted, amongst which, ETS proto‑oncogene 1 transcription factor (ETS1) was shown to be significantly associated with tumor invasion depth and negatively associated with miR‑200b expression. The interaction between miR‑200b and ETS1 was confirmed using a dual‑luciferase reporter assay. Using rescue experiments, the increased migratory ability of the miR‑200b‑overexpressing cells was reversed by ETS1 overexpression. In summary, this study showed that miR‑200b overexpression serves a carcinogenic role and promotes the migration of BEAS‑2B cells following long‑term exposure to CS by targeting ETS1. |
Databáze: | OpenAIRE |
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