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Article

Fra-1 is upregulated in lung cancer tissues and inhibits the apoptosis of lung cancer cells by the P53 signaling pathway

  • Authors:
    • Guangwei Zhong
    • Xi Chen
    • Xia Fang
    • Dongsheng Wang
    • Mingxuan Xie
    • Qiong Chen
  • View Affiliations / Copyright

    Affiliations: Institute of Integrated Traditional Chinese and Western Medicine, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China, Department of Geriatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China
  • Pages: 447-453
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    Published online on: November 4, 2015
       https://doi.org/10.3892/or.2015.4395
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Abstract

Fos-related antigen-1 (Fra-1) is a member of the activator protein-1 transcription factor superfamily. It plays important roles in oncogenesis in various types of malignancies. Herein, we investigated the expression of Fra-1 in lung cancer tissues by qPCR, immunohistochemistry, and western blot technologies. The results showed that Fra-1 was overexpressed in the lung cancer tissues when compared with the level in the adjacent non‑cancerous tissues. To explore the possible mechanism of Fra-1 in lung cancer, we elucidated the effect of Fra-1 on the apoptosis of lung cancer H460 cells, and found that the rate of cell apoptosis was decreased in the H460/Fra-1 cells compared with the H460 or H460/vector cells. Cell apoptosis is closely related with a reduction in mitochondrial membrane potential (ΔΨm) and an increase in intracellular reactive oxygen species (ROS) and calcium ion (Ca2+) concentrations. Our results showed that overexpression of Fra-1 in the lung cancer H460 cells, led to an increase in ΔΨm and and a decrease in intracellular ROS and Ca2+ concentrations. Furthermore, we found that Fra-1 was correlated with dysregulation of the P53 signaling pathway in lung cancer tissues in vitro. At the same time, we found that Fra-1 overexpression affected the expression of MDM2 and P53 in vivo. In summary, our results suggest that Fra-1 is upregulated in lung cancer tissues and functions by affecting the P53 signaling pathway in lung cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Zhong G, Chen X, Fang X, Wang D, Xie M and Chen Q: Fra-1 is upregulated in lung cancer tissues and inhibits the apoptosis of lung cancer cells by the P53 signaling pathway. Oncol Rep 35: 447-453, 2016.
APA
Zhong, G., Chen, X., Fang, X., Wang, D., Xie, M., & Chen, Q. (2016). Fra-1 is upregulated in lung cancer tissues and inhibits the apoptosis of lung cancer cells by the P53 signaling pathway. Oncology Reports, 35, 447-453. https://doi.org/10.3892/or.2015.4395
MLA
Zhong, G., Chen, X., Fang, X., Wang, D., Xie, M., Chen, Q."Fra-1 is upregulated in lung cancer tissues and inhibits the apoptosis of lung cancer cells by the P53 signaling pathway". Oncology Reports 35.1 (2016): 447-453.
Chicago
Zhong, G., Chen, X., Fang, X., Wang, D., Xie, M., Chen, Q."Fra-1 is upregulated in lung cancer tissues and inhibits the apoptosis of lung cancer cells by the P53 signaling pathway". Oncology Reports 35, no. 1 (2016): 447-453. https://doi.org/10.3892/or.2015.4395
Copy and paste a formatted citation
x
Spandidos Publications style
Zhong G, Chen X, Fang X, Wang D, Xie M and Chen Q: Fra-1 is upregulated in lung cancer tissues and inhibits the apoptosis of lung cancer cells by the P53 signaling pathway. Oncol Rep 35: 447-453, 2016.
APA
Zhong, G., Chen, X., Fang, X., Wang, D., Xie, M., & Chen, Q. (2016). Fra-1 is upregulated in lung cancer tissues and inhibits the apoptosis of lung cancer cells by the P53 signaling pathway. Oncology Reports, 35, 447-453. https://doi.org/10.3892/or.2015.4395
MLA
Zhong, G., Chen, X., Fang, X., Wang, D., Xie, M., Chen, Q."Fra-1 is upregulated in lung cancer tissues and inhibits the apoptosis of lung cancer cells by the P53 signaling pathway". Oncology Reports 35.1 (2016): 447-453.
Chicago
Zhong, G., Chen, X., Fang, X., Wang, D., Xie, M., Chen, Q."Fra-1 is upregulated in lung cancer tissues and inhibits the apoptosis of lung cancer cells by the P53 signaling pathway". Oncology Reports 35, no. 1 (2016): 447-453. https://doi.org/10.3892/or.2015.4395
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