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Article

MicroRNA‑26a regulates ANXA1, rather than DAL‑1, in the development of lung cancer

  • Authors:
    • Tonghui Cai
    • Xiaoying  Guan
    • Hongyan  Wang
    • Ying  Fang
    • Jie  Long
    • Xiaobin  Xie
    • Yajie  Zhang
  • View Affiliations / Copyright

    Affiliations: Department of Pathology, Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510150, P.R. China, Department of Pathology, School of Basic Medical Science, Guangzhou Medical University, Guangzhou, Guangdong 511436, P.R. China
  • Pages: 5893-5902
    |
    Published online on: February 14, 2018
       https://doi.org/10.3892/ol.2018.8048
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Abstract

The aim of the present study was to investigate the expression and role of microRNA‑26a (miR‑26a) in lung cancer, and to verify whether differentially expressed in adenocarcinoma of the lung (DAL‑1) is the target protein of miR‑26a. mRNA expression levels of miR‑26a and DAL‑1 were detected using reverse transcription‑quantitative polymerase chain reaction. Protein expression levels of DAL‑1 and annexin A1 (ANXA1) were evaluated by western blot analysis. Cell Counting Kit‑8, Transwell and wound scratch healing assays were used to characterize the function of miR‑26a in lung cancer cells. The association of DAL‑1 with miR‑26a or ANXA1 was determined by dual‑luciferase reporter or two‑dimensional gel electrophoresis assays. miR‑26a revealed decreased expression levels in lung cancer tissues compared with normal lung tissues, and decreased expression levels in lung cancer cells compared with 16HBE cells. Inhibition of miR‑26a promoted lung cancer cell growth, migration and invasion. The DAL‑1 protein exhibited downregulated expression levels in lung cancer tissues. DAL‑1 was not the direct target gene of miR‑26a. The two‑dimensional gel electrophoresis assay confirmed that DAL‑1 and ANXA1 were associated proteins. Expression levels of the ANXA1 protein were increased following DAL‑1 gene silencing. The altered expression level of miR‑26a affected the expression of ANXA1, and not of DAL‑1. miR‑26a demonstrated decreased expression levels in lung cancer cells, and it has an important effect on the biological function of lung cancer cells. However, DAL‑1 was not a target gene of miR‑26a. As a DAL‑1 associated protein, ANXA1 was regulated by miR‑26a.
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Copy and paste a formatted citation
Spandidos Publications style
Cai T, Guan X, Wang H, Fang Y, Long J, Xie X and Zhang Y: MicroRNA‑26a regulates ANXA1, rather than DAL‑1, in the development of lung cancer. Oncol Lett 15: 5893-5902, 2018.
APA
Cai, T., Guan, X., Wang, H., Fang, Y., Long, J., Xie, X., & Zhang, Y. (2018). MicroRNA‑26a regulates ANXA1, rather than DAL‑1, in the development of lung cancer. Oncology Letters, 15, 5893-5902. https://doi.org/10.3892/ol.2018.8048
MLA
Cai, T., Guan, X., Wang, H., Fang, Y., Long, J., Xie, X., Zhang, Y."MicroRNA‑26a regulates ANXA1, rather than DAL‑1, in the development of lung cancer". Oncology Letters 15.4 (2018): 5893-5902.
Chicago
Cai, T., Guan, X., Wang, H., Fang, Y., Long, J., Xie, X., Zhang, Y."MicroRNA‑26a regulates ANXA1, rather than DAL‑1, in the development of lung cancer". Oncology Letters 15, no. 4 (2018): 5893-5902. https://doi.org/10.3892/ol.2018.8048
Copy and paste a formatted citation
x
Spandidos Publications style
Cai T, Guan X, Wang H, Fang Y, Long J, Xie X and Zhang Y: MicroRNA‑26a regulates ANXA1, rather than DAL‑1, in the development of lung cancer. Oncol Lett 15: 5893-5902, 2018.
APA
Cai, T., Guan, X., Wang, H., Fang, Y., Long, J., Xie, X., & Zhang, Y. (2018). MicroRNA‑26a regulates ANXA1, rather than DAL‑1, in the development of lung cancer. Oncology Letters, 15, 5893-5902. https://doi.org/10.3892/ol.2018.8048
MLA
Cai, T., Guan, X., Wang, H., Fang, Y., Long, J., Xie, X., Zhang, Y."MicroRNA‑26a regulates ANXA1, rather than DAL‑1, in the development of lung cancer". Oncology Letters 15.4 (2018): 5893-5902.
Chicago
Cai, T., Guan, X., Wang, H., Fang, Y., Long, J., Xie, X., Zhang, Y."MicroRNA‑26a regulates ANXA1, rather than DAL‑1, in the development of lung cancer". Oncology Letters 15, no. 4 (2018): 5893-5902. https://doi.org/10.3892/ol.2018.8048
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