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Article

Overexpression of ROD1 inhibits invasion of breast cancer cells by suppressing the translocation of β‑catenin into the nucleus

  • Authors:
    • Ya Zhou
    • Hanqing Zou
    • Enhao Wu
    • Lei Huang
    • Rui Yin
    • Yuxin Mei
    • Xun Zhu
  • View Affiliations / Copyright

    Affiliations: Department of General Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, P.R. China
  • Pages: 2645-2653
    |
    Published online on: June 6, 2018
       https://doi.org/10.3892/ol.2018.8917
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Abstract

The incidence of breast cancer is increasing throughout the world. Although significant progress has been made in diagnostic techniques and targeted therapies, the prognosis of breast cancer remains poor. Regulator of differentiation 1 (ROD1) may inhibit the development of several types of cancer. However, the role of ROD1 in breast cancer cells remains unknown. In the present study, western blot analysis and reverse transcription‑quantitative polymerase chain reaction revealed that expression of ROD1 was significantly reduced in breast cancer cells. Overexpression of ROD1 reduced the proliferation rate, demonstrated using a Cell Counting Kit‑8 assay. Additionally, the overexpression of ROD1 decreased the invasiveness of breast cancer cells, indicating that ROD1 may serve as a tumor suppressor. Additionally, the data suggested that ROD1 significantly suppressed the activity of Wnt luciferase reporter (TOP Flash) in MDA‑MB‑231 cells. Furthermore, it was demonstrated that ROD1 may interact with β‑catenin by using co‑immunoprecipitation, resulting in suppression of β‑catenin migration into the nucleus. Notably, ROD1 demonstrated its anticancer effect by decreasing β‑catenin (Y333) phosphorylation in a nude mouse xenograft model. Overexpression of ROD1 may downregulate Ki67 protein levels, as determined by immunohistochemistry. These results indicated that ROD1 may be used as a therapeutic target in patients with breast cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Zhou Y, Zou H, Wu E, Huang L, Yin R, Mei Y and Zhu X: Overexpression of ROD1 inhibits invasion of breast cancer cells by suppressing the translocation of β‑catenin into the nucleus. Oncol Lett 16: 2645-2653, 2018.
APA
Zhou, Y., Zou, H., Wu, E., Huang, L., Yin, R., Mei , Y., & Zhu, X. (2018). Overexpression of ROD1 inhibits invasion of breast cancer cells by suppressing the translocation of β‑catenin into the nucleus. Oncology Letters, 16, 2645-2653. https://doi.org/10.3892/ol.2018.8917
MLA
Zhou, Y., Zou, H., Wu, E., Huang, L., Yin, R., Mei , Y., Zhu, X."Overexpression of ROD1 inhibits invasion of breast cancer cells by suppressing the translocation of β‑catenin into the nucleus". Oncology Letters 16.2 (2018): 2645-2653.
Chicago
Zhou, Y., Zou, H., Wu, E., Huang, L., Yin, R., Mei , Y., Zhu, X."Overexpression of ROD1 inhibits invasion of breast cancer cells by suppressing the translocation of β‑catenin into the nucleus". Oncology Letters 16, no. 2 (2018): 2645-2653. https://doi.org/10.3892/ol.2018.8917
Copy and paste a formatted citation
x
Spandidos Publications style
Zhou Y, Zou H, Wu E, Huang L, Yin R, Mei Y and Zhu X: Overexpression of ROD1 inhibits invasion of breast cancer cells by suppressing the translocation of β‑catenin into the nucleus. Oncol Lett 16: 2645-2653, 2018.
APA
Zhou, Y., Zou, H., Wu, E., Huang, L., Yin, R., Mei , Y., & Zhu, X. (2018). Overexpression of ROD1 inhibits invasion of breast cancer cells by suppressing the translocation of β‑catenin into the nucleus. Oncology Letters, 16, 2645-2653. https://doi.org/10.3892/ol.2018.8917
MLA
Zhou, Y., Zou, H., Wu, E., Huang, L., Yin, R., Mei , Y., Zhu, X."Overexpression of ROD1 inhibits invasion of breast cancer cells by suppressing the translocation of β‑catenin into the nucleus". Oncology Letters 16.2 (2018): 2645-2653.
Chicago
Zhou, Y., Zou, H., Wu, E., Huang, L., Yin, R., Mei , Y., Zhu, X."Overexpression of ROD1 inhibits invasion of breast cancer cells by suppressing the translocation of β‑catenin into the nucleus". Oncology Letters 16, no. 2 (2018): 2645-2653. https://doi.org/10.3892/ol.2018.8917
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