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April-2015 Volume 33 Issue 4

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Article

Angiomotin promotes breast cancer cell proliferation and invasion

  • Authors:
    • Meng Lv
    • Meiling Lv
    • Ling Chen
    • Tianjie Qin
    • Xiao Zhang
    • Peijun Liu
    • Jin Yang
  • View Affiliations / Copyright

    Affiliations: Department of Oncology, The First Affiliated Hospital, Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710061, P.R. China, Center for Translational Medicine, The First Affiliated Hospital, Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710061, P.R. China
  • Pages: 1938-1946
    |
    Published online on: February 3, 2015
       https://doi.org/10.3892/or.2015.3780
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Abstract

Angiomotin (Amot) is a multifunctional protein involved in endothelial cell migration and tube formation and angiogenesis. However, the biological role and molecular mechanism for the abnormal expression of Amot in breast cancer is poorly understood. The aim of the present study was to examine the function of and relationship between Amot and the Hippo-Yes-associated protein (YAP) pathway. The expression and location of Amot was examined in breast cancer tissues and cell lines using immunohistochemistry, real-time polymerase chain reaction analysis (RT-PCR), western blotting and immunofluorescence. ANOVA, Student's t-test, Wilcoxon and Chi-square tests were utilized to determine the association of Amot expression with clinically relevant parameters. Stable Amot knockdown MCF-7 cells (MCF-7 Amot KD) were generated to investigate the impact of Amot downregulation on the growth and invasion of MCF-7 cells in vitro. Western blotting was applied to detect the expression of the Hippo-YAP pathway protein in the MCF-7 cells. It was observed that Amot was highly expressed in breast cancer tissues, but weakly expressed in adjacent non-cancerous tissues. Additionally, the expression level of Amot was correlated with that of Ki-67. In MCF-7 cells, Amot downregulation resulted in a significant decrease of cell proliferation and invasiveness. Following Amot knockdown in MCF-7 cells, the expression of YAP, YAP/TAZ and LATS1 was decreased. In particular, the expression of YAP was markedly reduced in the nucleoprotein. The results suggested that Amot was highly expressed in breast cancer tissues and was important in the promotion of breast cancer cell proliferation and invasion. In addition, there was a more intimate connection between Amot and Hippo-YAP pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Lv M, Lv M, Chen L, Qin T, Zhang X, Liu P and Yang J: Angiomotin promotes breast cancer cell proliferation and invasion. Oncol Rep 33: 1938-1946, 2015.
APA
Lv, M., Lv, M., Chen, L., Qin, T., Zhang, X., Liu, P., & Yang, J. (2015). Angiomotin promotes breast cancer cell proliferation and invasion. Oncology Reports, 33, 1938-1946. https://doi.org/10.3892/or.2015.3780
MLA
Lv, M., Lv, M., Chen, L., Qin, T., Zhang, X., Liu, P., Yang, J."Angiomotin promotes breast cancer cell proliferation and invasion". Oncology Reports 33.4 (2015): 1938-1946.
Chicago
Lv, M., Lv, M., Chen, L., Qin, T., Zhang, X., Liu, P., Yang, J."Angiomotin promotes breast cancer cell proliferation and invasion". Oncology Reports 33, no. 4 (2015): 1938-1946. https://doi.org/10.3892/or.2015.3780
Copy and paste a formatted citation
x
Spandidos Publications style
Lv M, Lv M, Chen L, Qin T, Zhang X, Liu P and Yang J: Angiomotin promotes breast cancer cell proliferation and invasion. Oncol Rep 33: 1938-1946, 2015.
APA
Lv, M., Lv, M., Chen, L., Qin, T., Zhang, X., Liu, P., & Yang, J. (2015). Angiomotin promotes breast cancer cell proliferation and invasion. Oncology Reports, 33, 1938-1946. https://doi.org/10.3892/or.2015.3780
MLA
Lv, M., Lv, M., Chen, L., Qin, T., Zhang, X., Liu, P., Yang, J."Angiomotin promotes breast cancer cell proliferation and invasion". Oncology Reports 33.4 (2015): 1938-1946.
Chicago
Lv, M., Lv, M., Chen, L., Qin, T., Zhang, X., Liu, P., Yang, J."Angiomotin promotes breast cancer cell proliferation and invasion". Oncology Reports 33, no. 4 (2015): 1938-1946. https://doi.org/10.3892/or.2015.3780
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