Carcinogenesis, Teratogenesis & Mutagenesis ›› 2017, Vol. 29 ›› Issue (6): 422-426.doi: 10.3969/j.issn.1004-616x.2017.06.004

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Expression of LncRNA EMX2OS during glycidyl methacrylate-induced malignant transformation of 16HBE cells

WANG Quankai1,2, WANG Boshen3, XIE Guangyun1,2, KANG Tongying1,2, ZHU Baoli3, XU Jianning1,2   

  1. 1. National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050;
    2. Key Laboratory of Chemical Safety and Health, Chinese Center for Disease Control and Prevention, Beijing 100050;
    3. Jiangsu Center for Disease Control and Prevention, Nanjing 210009, Jiangsu, China
  • Received:2017-07-09 Revised:2017-09-19 Online:2017-11-30 Published:2017-11-30

Abstract: OBJECTIVE:To investigate the expression of long non-coding RNA EMX2OS (LncRNA EMX2OS) during glycidyl methacrylate (GMA)-induced malignant transformation of 16HBE cells. METHODS:Malignantly transformed 16HBE cells (induced by exposure to 8 μg/mL GMA) and solvent control cells (exposed to DMSO) at around the 30th generation were harvested. High throughput LncRNA microarrays were used to detect differences in expression profile of LncRNAs between the two groups of cells. Changes in LncRNAs were screened through strategies such as fold changes and neighboring genes analyses. Real-time fluorescence quantitative PCR (qPCR) and gene chip were applied to measure the expression levels of LncRNA EMX2OS and EMX2,respectively. RESULTS:Based on the result of LncRNA microarrays,expressions of LncRNA EMX2OS was up-regulated by 6.01 fold in the transformed cells campared to the control cells. In addition, qPCR analyses showed that LncRNA EMX2OS increased 3.37 fold and EMX2 increased 1.88 fold change (P < 0.05). The trends of increase in EMX2 and EMX2OS trends were identical. CONCLUSION:GMA induced significant increase in expression of LncRNA EMX2OS of 16HBE cells and the expression can be considered as a specific biomarker which is involved in GMA-induced malignant transformation 16HBE cells.

Key words: glycidyl methacrylate, human bronchial epithelial cells, LncRNA EMX2OS, EMX2

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