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Article Open Access

miR-21 and KLF4 jointly augment epithelial‑mesenchymal transition via the Akt/ERK1/2 pathway

  • Authors:
    • Chen-Hai Liu
    • Qiang Huang
    • Zhi-Yuan Jin
    • Cheng-Lin Zhu
    • Zhen Liu
    • Chao Wang
  • View Affiliations / Copyright

    Affiliations: Department of General Surgery, Anhui Provincial Hospital of Anhui Medical University, Anhui Key Laboratory of Hepatopancreatobiliary Surgery, Hefei, Anhui 230001, P.R. China
    Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1109-1115
    |
    Published online on: February 14, 2017
       https://doi.org/10.3892/ijo.2017.3876
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Abstract

miR-21 induces epithelial-mesenchymal transition (EMT) of human cholangiocarcinoma (CCA) cells. However, the mechanism by which this occurs remains unclear. In the present study, high throughput platform was employed to detect the genes that are differential expressed in QBC939 cells transfected with a hsa-miR-21 antagomir or control vectors. The EMT-related Krüppel-like factor 4 (KLF4) gene was downregulated after miR-21 was knocked down. Overexpression of miR-21 upregulated KLF4, Akt, ERK and mesenchymal cell markers (N-cadherin and vimentin), downregulated the expression of epithelial cell marker E-cadherin and reduced cell migration and invasion. Immunohistochemistry showed that KLF4, pAkt and pERK were upregulated in tumor xenografts transfected with miR-21 mimics. Inhibitors of the PI3K-Akt and ERK1/2 pathways, LY294002 and U0126, significantly suppressed the EMT phenotype. The present data demonstrated that overexpression of miR-21, accompanied with KLF4, augmented the EMT via inactivation of Akt and ERK1/2 pathways. In conclusion, we have identified a novel mechanism that may be targeted in an attempt to relieve the malignant biological behavior of CCA cells.
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Copy and paste a formatted citation
Spandidos Publications style
Liu C, Huang Q, Jin Z, Zhu C, Liu Z and Wang C: miR-21 and KLF4 jointly augment epithelial‑mesenchymal transition via the Akt/ERK1/2 pathway. Int J Oncol 50: 1109-1115, 2017.
APA
Liu, C., Huang, Q., Jin, Z., Zhu, C., Liu, Z., & Wang, C. (2017). miR-21 and KLF4 jointly augment epithelial‑mesenchymal transition via the Akt/ERK1/2 pathway. International Journal of Oncology, 50, 1109-1115. https://doi.org/10.3892/ijo.2017.3876
MLA
Liu, C., Huang, Q., Jin, Z., Zhu, C., Liu, Z., Wang, C."miR-21 and KLF4 jointly augment epithelial‑mesenchymal transition via the Akt/ERK1/2 pathway". International Journal of Oncology 50.4 (2017): 1109-1115.
Chicago
Liu, C., Huang, Q., Jin, Z., Zhu, C., Liu, Z., Wang, C."miR-21 and KLF4 jointly augment epithelial‑mesenchymal transition via the Akt/ERK1/2 pathway". International Journal of Oncology 50, no. 4 (2017): 1109-1115. https://doi.org/10.3892/ijo.2017.3876
Copy and paste a formatted citation
x
Spandidos Publications style
Liu C, Huang Q, Jin Z, Zhu C, Liu Z and Wang C: miR-21 and KLF4 jointly augment epithelial‑mesenchymal transition via the Akt/ERK1/2 pathway. Int J Oncol 50: 1109-1115, 2017.
APA
Liu, C., Huang, Q., Jin, Z., Zhu, C., Liu, Z., & Wang, C. (2017). miR-21 and KLF4 jointly augment epithelial‑mesenchymal transition via the Akt/ERK1/2 pathway. International Journal of Oncology, 50, 1109-1115. https://doi.org/10.3892/ijo.2017.3876
MLA
Liu, C., Huang, Q., Jin, Z., Zhu, C., Liu, Z., Wang, C."miR-21 and KLF4 jointly augment epithelial‑mesenchymal transition via the Akt/ERK1/2 pathway". International Journal of Oncology 50.4 (2017): 1109-1115.
Chicago
Liu, C., Huang, Q., Jin, Z., Zhu, C., Liu, Z., Wang, C."miR-21 and KLF4 jointly augment epithelial‑mesenchymal transition via the Akt/ERK1/2 pathway". International Journal of Oncology 50, no. 4 (2017): 1109-1115. https://doi.org/10.3892/ijo.2017.3876
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