Open Access

Involvement of NF-κB activation in the cisplatin resistance of human epidermoid carcinoma KCP-4 cells

  • Authors:
    • Shigeru Oiso
    • Ryuji Ikeda
    • Kazuo Nakamura
    • Yasuo Takeda
    • Shin-Ichi Akiyama
    • Hiroko Kariyazono
  • View Affiliations

  • Published online on: May 4, 2012     https://doi.org/10.3892/or.2012.1801
  • Pages: 27-32
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Abstract

cis-Diamminedichloroplatinum II (cisplatin) is one of the most potent antitumor agents for the treatment of various types of cancer. In spite of its therapeutic usefulness, the intrinsic resistance acquired under continuous treatment limits its benefit in cancer therapy. KCP-4, a cisplatin-resistant cell line, was derived from human epidermoid carcinoma KB-3-1 cells. Since the accumulation of cisplatin in KCP-4 cells is markedly reduced by the presence of an efflux pump, this pump is thought to be related to cisplatin resistance of the KCP-4 cells. However, given that KCP-4 cells are tremendously resistant to cisplatin compared with KB-3-1 cells, it is possible that another mechanism exists. The aim of this study was to investigate whether the activation of nuclear factor-kappa B (NF-κB) contributes to the cisplatin resistance of KCP-4 cells. We used the level of translocated NF-κB into the nucleus, determined by immunoblot analysis, as the indicator of NF-κB activation. The activation level of NF-κB was higher in KCP-4 cells than in KB-3-1 cells. KCP-4 cells were treated with a combination of cisplatin and curcumin, an inhibitor of NF-κB activation, and the cell viabilities were subsequently determined by the MTT assay using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide. In the presence of 10 µmol/l curcumin, we found that the sensitivity of KCP-4 cells to 100 and 300 µmol/l cisplatin was augmented. Additionally, curcumin reduced the activation levels of NF-κB in KCP-4 cells, and suppressed the expression levels of Bcl-2, Bcl-xL and survivin, which are apoptosis-related proteins regulated by NF-κB. Our results suggest that the high cisplatin resistance of KCP-4 cells compared with KB-3-1 cells results from multiple mechanisms other than increased cisplatin efflux, including the activation of NF-κB.

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July 2012
Volume 28 Issue 1

Print ISSN: 1021-335X
Online ISSN:1791-2431

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Spandidos Publications style
Oiso S, Ikeda R, Nakamura K, Takeda Y, Akiyama S and Kariyazono H: Involvement of NF-κB activation in the cisplatin resistance of human epidermoid carcinoma KCP-4 cells. Oncol Rep 28: 27-32, 2012
APA
Oiso, S., Ikeda, R., Nakamura, K., Takeda, Y., Akiyama, S., & Kariyazono, H. (2012). Involvement of NF-κB activation in the cisplatin resistance of human epidermoid carcinoma KCP-4 cells. Oncology Reports, 28, 27-32. https://doi.org/10.3892/or.2012.1801
MLA
Oiso, S., Ikeda, R., Nakamura, K., Takeda, Y., Akiyama, S., Kariyazono, H."Involvement of NF-κB activation in the cisplatin resistance of human epidermoid carcinoma KCP-4 cells". Oncology Reports 28.1 (2012): 27-32.
Chicago
Oiso, S., Ikeda, R., Nakamura, K., Takeda, Y., Akiyama, S., Kariyazono, H."Involvement of NF-κB activation in the cisplatin resistance of human epidermoid carcinoma KCP-4 cells". Oncology Reports 28, no. 1 (2012): 27-32. https://doi.org/10.3892/or.2012.1801