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Effect of silencing SATB1 on proliferation, invasion and apoptosis of A549 human lung adenocarcinoma cells

  • Authors:
    • Bo Huang
    • Hongli Zhou
    • Siwang Wang
    • Xian Ping Lang
    • Xiaodong Wang
  • View Affiliations / Copyright

    Affiliations: Department of Thoracic Surgery, The First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121000, P.R. China, Department of Kidney Diseases, The First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning 121000, P.R. China
    Copyright: © Huang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 3818-3824
    |
    Published online on: September 22, 2016
       https://doi.org/10.3892/ol.2016.5179
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Abstract

The present study aimed to explore the clinical characteristics of special adenine‑thymine‑rich sequence‑binding protein 1 (SATB1) in lung adenocarcinoma and its role in the proliferation, invasion, migration and apoptosis of the lung adenocarcinoma cell line A549. The expression of SATB1 was first studied in tumor tissues of lung adenocarcinoma and adjacent non‑tumor tissues. The siRNA green fluorescent protein expression vector of SATB1 was constructed and transfected into the lung adenocarcinoma cell line A549, then a fluorescence microscope was used to study the transfection efficiency. Western blot analysis was adopted to measure the silencing efficiency. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Transwell and scratch assays were used to study cell proliferation, invasion and migration activity, and the apoptosis rate was tested by flow cytometry. SATB1 expression was low in the adjacent non‑tumor tissues but high in lung adenocarcinoma tissues, and it was reversely proportional to the differentiation degree. Following transfection with SATB1‑siRNA, the expression of SATB1 in A549 cells was blocked (P<0.01). In addition, the proliferation, invasion and migration abilities of cells decreased significantly while the apoptosis rate increased significantly (P<0.01). In conclusion SATB1 is closely associated with the patho­genesis and development of lung adenocarcinoma.
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Copy and paste a formatted citation
Spandidos Publications style
Huang B, Zhou H, Wang S, Lang XP and Wang X: Effect of silencing SATB1 on proliferation, invasion and apoptosis of A549 human lung adenocarcinoma cells. Oncol Lett 12: 3818-3824, 2016.
APA
Huang, B., Zhou, H., Wang, S., Lang, X.P., & Wang, X. (2016). Effect of silencing SATB1 on proliferation, invasion and apoptosis of A549 human lung adenocarcinoma cells. Oncology Letters, 12, 3818-3824. https://doi.org/10.3892/ol.2016.5179
MLA
Huang, B., Zhou, H., Wang, S., Lang, X. P., Wang, X."Effect of silencing SATB1 on proliferation, invasion and apoptosis of A549 human lung adenocarcinoma cells". Oncology Letters 12.5 (2016): 3818-3824.
Chicago
Huang, B., Zhou, H., Wang, S., Lang, X. P., Wang, X."Effect of silencing SATB1 on proliferation, invasion and apoptosis of A549 human lung adenocarcinoma cells". Oncology Letters 12, no. 5 (2016): 3818-3824. https://doi.org/10.3892/ol.2016.5179
Copy and paste a formatted citation
x
Spandidos Publications style
Huang B, Zhou H, Wang S, Lang XP and Wang X: Effect of silencing SATB1 on proliferation, invasion and apoptosis of A549 human lung adenocarcinoma cells. Oncol Lett 12: 3818-3824, 2016.
APA
Huang, B., Zhou, H., Wang, S., Lang, X.P., & Wang, X. (2016). Effect of silencing SATB1 on proliferation, invasion and apoptosis of A549 human lung adenocarcinoma cells. Oncology Letters, 12, 3818-3824. https://doi.org/10.3892/ol.2016.5179
MLA
Huang, B., Zhou, H., Wang, S., Lang, X. P., Wang, X."Effect of silencing SATB1 on proliferation, invasion and apoptosis of A549 human lung adenocarcinoma cells". Oncology Letters 12.5 (2016): 3818-3824.
Chicago
Huang, B., Zhou, H., Wang, S., Lang, X. P., Wang, X."Effect of silencing SATB1 on proliferation, invasion and apoptosis of A549 human lung adenocarcinoma cells". Oncology Letters 12, no. 5 (2016): 3818-3824. https://doi.org/10.3892/ol.2016.5179
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