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Article Open Access

Nek2-targeted ASO or siRNA pretreatment enhances anticancer drug sensitivity in triple‑negative breast cancer cells

  • Authors:
    • Jaehyung Lee
    • Lauren Gollahon
  • View Affiliations / Copyright

    Affiliations: Department of Biological Sciences, Texas Tech University, Lubbock, TX, USA
    Copyright: © Lee et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].
  • Pages: 839-847
    |
    Published online on: January 22, 2013
       https://doi.org/10.3892/ijo.2013.1788
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Abstract

Although the anticancer drugs paclitaxel and doxorubicin are commonly used to treat many solid tumors, their effectiveness is highly variable due to tumor cell resistance. Therefore, it is important to find mechanisms that can be targeted to increase the sensitivity of cancer cells to current chemotherapeutic agents. NIMA‑related kinase 2 (Nek2), a serine/threonine kinase is emerging as an important oncogene because of its regulatory role in mitosis. Thus, regulation of the Nek2 expression levels may prove important as a target for cancer treatment. The purpose of our study was to determine whether drug sensitivity was increased in the triple negative breast cancer cell lines MDA-MB-231 and MDA-MB-468 by using small interfering RNA (siRNA) and antisense oligonucleotides (ASOs) against Nek2. To this end, MDA-MB-231 and MDA-MB-468 breast cancer cells transfected with Nek2 siRNA or ASO were exposed to various concentrations of paclitaxel and doxorubicin. Cell viability, cell cycle distribution and apoptosis were evaluated. We observed that drug susceptibility in these transfected cells was dramatically increased compared with either agent alone. FACS results showed that apoptosis was induced in siRNA- and ASO‑transfected cells as expected due to the regulatory function of Nek2 in centrosome duplication. Interestingly, the cell cyle was not arrested in transfected cells. We found that siRNA and ASO against Nek2 worked synergistically with paclitaxel and doxorubicin by promoting cell apoptosis. Our results suggest that these drugs in combination with Nek2 siRNA or ASO treatment may improve the sensitivity of cancer cells during chemotherapy treatments.
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Copy and paste a formatted citation
Spandidos Publications style
Lee J and Gollahon L: Nek2-targeted ASO or siRNA pretreatment enhances anticancer drug sensitivity in triple‑negative breast cancer cells. Int J Oncol 42: 839-847, 2013.
APA
Lee, J., & Gollahon, L. (2013). Nek2-targeted ASO or siRNA pretreatment enhances anticancer drug sensitivity in triple‑negative breast cancer cells. International Journal of Oncology, 42, 839-847. https://doi.org/10.3892/ijo.2013.1788
MLA
Lee, J., Gollahon, L."Nek2-targeted ASO or siRNA pretreatment enhances anticancer drug sensitivity in triple‑negative breast cancer cells". International Journal of Oncology 42.3 (2013): 839-847.
Chicago
Lee, J., Gollahon, L."Nek2-targeted ASO or siRNA pretreatment enhances anticancer drug sensitivity in triple‑negative breast cancer cells". International Journal of Oncology 42, no. 3 (2013): 839-847. https://doi.org/10.3892/ijo.2013.1788
Copy and paste a formatted citation
x
Spandidos Publications style
Lee J and Gollahon L: Nek2-targeted ASO or siRNA pretreatment enhances anticancer drug sensitivity in triple‑negative breast cancer cells. Int J Oncol 42: 839-847, 2013.
APA
Lee, J., & Gollahon, L. (2013). Nek2-targeted ASO or siRNA pretreatment enhances anticancer drug sensitivity in triple‑negative breast cancer cells. International Journal of Oncology, 42, 839-847. https://doi.org/10.3892/ijo.2013.1788
MLA
Lee, J., Gollahon, L."Nek2-targeted ASO or siRNA pretreatment enhances anticancer drug sensitivity in triple‑negative breast cancer cells". International Journal of Oncology 42.3 (2013): 839-847.
Chicago
Lee, J., Gollahon, L."Nek2-targeted ASO or siRNA pretreatment enhances anticancer drug sensitivity in triple‑negative breast cancer cells". International Journal of Oncology 42, no. 3 (2013): 839-847. https://doi.org/10.3892/ijo.2013.1788
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