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Article Open Access

FAK regulates epithelial‑mesenchymal transition in adenomyosis

  • Authors:
    • Dexuan Zheng
    • Hua Duan
    • Sha Wang
    • Qian Xu
    • Lu Gan
    • Jinjiao Li
    • Qianjing Dong
  • View Affiliations / Copyright

    Affiliations: Department of Gynecology Minimally Invasive Center, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing 100000, P.R. China
    Copyright: © Zheng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 5461-5472
    |
    Published online on: October 26, 2018
       https://doi.org/10.3892/mmr.2018.9600
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Abstract

Epithelial‑mesenchymal transition (EMT) has been associated with the pathogenesis of adenomyosis; focal adhesion kinase (FAK) serves an important role in the EMT process. The aim of the present study was to determine whether FAK regulates EMT in adenomyosis and to investigate the potential pathway in this process. The expression of FAK and EMT‑associated molecules in adenomyosis and control cells were determined by immunohistochemical staining and immunofluorescence at the protein level, and at the mRNA level by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Small interfering RNAs were designed to knock down FAK expression. Subsequently, molecular expression was detected by immunofluorescence, RT‑qPCR and western blotting; cell migration was investigated via Transwell assays. In addition, the expression levels of members of the phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT) signaling pathway was also analyzed by RT‑qPCR and western blotting to determine the association between these members and EMT in adenomyosis. The results of the present study revealed that FAK was upregulated and the expression levels of EMT‑associated molecules were altered in adenomyosis. Silencing FAK expression inhibited adenomyosis cell migration in vitro and the expression of EMT‑promoting molecules, suggesting that the FAK/PI3K/AKT signaling pathway may participate in the EMT of endometrial cells in adenomyosis. In conclusion, FAK may regulate EMT in adenomyosis, and this process may be associated with the PI3K/AKT signaling pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Zheng D, Duan H, Wang S, Xu Q, Gan L, Li J and Dong Q: FAK regulates epithelial‑mesenchymal transition in adenomyosis. Mol Med Rep 18: 5461-5472, 2018.
APA
Zheng, D., Duan, H., Wang, S., Xu, Q., Gan, L., Li, J., & Dong, Q. (2018). FAK regulates epithelial‑mesenchymal transition in adenomyosis. Molecular Medicine Reports, 18, 5461-5472. https://doi.org/10.3892/mmr.2018.9600
MLA
Zheng, D., Duan, H., Wang, S., Xu, Q., Gan, L., Li, J., Dong, Q."FAK regulates epithelial‑mesenchymal transition in adenomyosis". Molecular Medicine Reports 18.6 (2018): 5461-5472.
Chicago
Zheng, D., Duan, H., Wang, S., Xu, Q., Gan, L., Li, J., Dong, Q."FAK regulates epithelial‑mesenchymal transition in adenomyosis". Molecular Medicine Reports 18, no. 6 (2018): 5461-5472. https://doi.org/10.3892/mmr.2018.9600
Copy and paste a formatted citation
x
Spandidos Publications style
Zheng D, Duan H, Wang S, Xu Q, Gan L, Li J and Dong Q: FAK regulates epithelial‑mesenchymal transition in adenomyosis. Mol Med Rep 18: 5461-5472, 2018.
APA
Zheng, D., Duan, H., Wang, S., Xu, Q., Gan, L., Li, J., & Dong, Q. (2018). FAK regulates epithelial‑mesenchymal transition in adenomyosis. Molecular Medicine Reports, 18, 5461-5472. https://doi.org/10.3892/mmr.2018.9600
MLA
Zheng, D., Duan, H., Wang, S., Xu, Q., Gan, L., Li, J., Dong, Q."FAK regulates epithelial‑mesenchymal transition in adenomyosis". Molecular Medicine Reports 18.6 (2018): 5461-5472.
Chicago
Zheng, D., Duan, H., Wang, S., Xu, Q., Gan, L., Li, J., Dong, Q."FAK regulates epithelial‑mesenchymal transition in adenomyosis". Molecular Medicine Reports 18, no. 6 (2018): 5461-5472. https://doi.org/10.3892/mmr.2018.9600
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