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Article

Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells

  • Authors:
    • Tao Zhang
    • Guannan Zhao
    • Chuanhe Yang
    • Peixin Dong
    • Hidemichi Watari
    • Lin Zeng
    • Lawrence M. Pfeffer
    • Junming Yue
  • View Affiliations / Copyright

    Affiliations: Laboratory Animal Center of The Academy of Military Medical Science, Beijing 100071, P.R. China, Center for Cancer Research, The University of Tennessee Health Science Center, Memphis, TN 38163, USA, Department of Women's Health Educational System, Hokkaido University, Sapporo, Hokkaido 060-0808, Japan
  • Pages: 4432-4438
    |
    Published online on: January 22, 2018
       https://doi.org/10.3892/ol.2018.7834
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Abstract

Ovarian cancer is one of the most common malignancies in women and has a high mortality rate due to metastatic progression and tumor recurrence. ASAP1 (ArfGAP with SH3 Domain, Ankyrin Repeat and PH Domain 1) is an ADP‑ribosylation factor GTPase-activating protein, which is involved in tumor metastasis. However, the role of ASAP1 in ovarian cancer is completely unknown. The present study reported that ASAP1 was highly expressed in ovarian carcinoma, and expression positively‑correlated with overall poor survival and prognosis of patients. Lentiviral vector mediated ASAP1 expression promoted cell migration and invasion in ovarian cancer cell lines SKOV3 and OVCAR3. In addition, ASAP1 promoted cell proliferation, survival and inhibited chemotherapy drug paclitaxel‑induced cell apoptosis. Furthermore, ASAP1 expression promoted epithelial to mesenchymal transition (EMT) by upregulating the mesenchymal cell markers N‑cadherin and vimentin, and downregulating epithelial cell marker E‑cadherin in the ovarian cancer cell lines. The data indicate for the first time that ASAP1 exhibits an oncogenic role by promoting EMT in ovarian cancer cells.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang T, Zhao G, Yang C, Dong P, Watari H, Zeng L, Pfeffer LM and Yue J: Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells. Oncol Lett 15: 4432-4438, 2018.
APA
Zhang, T., Zhao, G., Yang, C., Dong, P., Watari, H., Zeng, L. ... Yue, J. (2018). Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells. Oncology Letters, 15, 4432-4438. https://doi.org/10.3892/ol.2018.7834
MLA
Zhang, T., Zhao, G., Yang, C., Dong, P., Watari, H., Zeng, L., Pfeffer, L. M., Yue, J."Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells". Oncology Letters 15.4 (2018): 4432-4438.
Chicago
Zhang, T., Zhao, G., Yang, C., Dong, P., Watari, H., Zeng, L., Pfeffer, L. M., Yue, J."Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells". Oncology Letters 15, no. 4 (2018): 4432-4438. https://doi.org/10.3892/ol.2018.7834
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang T, Zhao G, Yang C, Dong P, Watari H, Zeng L, Pfeffer LM and Yue J: Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells. Oncol Lett 15: 4432-4438, 2018.
APA
Zhang, T., Zhao, G., Yang, C., Dong, P., Watari, H., Zeng, L. ... Yue, J. (2018). Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells. Oncology Letters, 15, 4432-4438. https://doi.org/10.3892/ol.2018.7834
MLA
Zhang, T., Zhao, G., Yang, C., Dong, P., Watari, H., Zeng, L., Pfeffer, L. M., Yue, J."Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells". Oncology Letters 15.4 (2018): 4432-4438.
Chicago
Zhang, T., Zhao, G., Yang, C., Dong, P., Watari, H., Zeng, L., Pfeffer, L. M., Yue, J."Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells". Oncology Letters 15, no. 4 (2018): 4432-4438. https://doi.org/10.3892/ol.2018.7834
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