Open Access

The role of katanin p60 in breast cancer bone metastasis

  • Authors:
    • Wenrong Fu
    • Hui Wu
    • Zhengjiang Cheng
    • Shaojun Huang
    • Hui Rao
  • View Affiliations

  • Published online on: February 2, 2018     https://doi.org/10.3892/ol.2018.7942
  • Pages: 4963-4969
  • Copyright: © Fu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

p60 is a subunit of katanin involved in microtubule‑severing. Previous studies of p60 were primarily focused on microtubule regulation and cell cycle regulation. More recent research has demonstrated that katanin p60 possesses a function in prostate cancer bone metastasis; however, its role in breast cancer bone metastasis remains unclear. In the present study, immunohistochemistry was used to analyze the expression of katanin p60 in primary and bone metastatic breast cancer. The role of up‑ and downregulated katanin p60 was investigated using cell proliferation, and migration experiments. Overall, katanin p60 was highly expressed in breast cancer bone metastatic tissue compared with primary tumor tissue. In breast cancer cells, overexpression of katanin p60 inhibited cell proliferation, but promoted cell migration, whereas silencing katanin p60 expression promoted cell proliferation but inhibited cell migration. Overall, the present study indicated that katanin p60 serves a role in cell proliferation and migration, and thus may be a novel therapeutic target for prevention of breast cancer metastasis.

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April 2018
Volume 15 Issue 4

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Online ISSN:1792-1082

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APA
Fu, W., Wu, H., Cheng, Z., Huang, S., & Rao, H. (2018). The role of katanin p60 in breast cancer bone metastasis. Oncology Letters, 15, 4963-4969. https://doi.org/10.3892/ol.2018.7942
MLA
Fu, W., Wu, H., Cheng, Z., Huang, S., Rao, H."The role of katanin p60 in breast cancer bone metastasis". Oncology Letters 15.4 (2018): 4963-4969.
Chicago
Fu, W., Wu, H., Cheng, Z., Huang, S., Rao, H."The role of katanin p60 in breast cancer bone metastasis". Oncology Letters 15, no. 4 (2018): 4963-4969. https://doi.org/10.3892/ol.2018.7942