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COX-2 inhibits anoikis by activation of the PI-3K/Akt pathway in human bladder cancer cells

Experimental & Molecular Medicine volume 37, pages199–203(2005)Cite this article

Abstract

Cyclooxygenase-2 (COX-2) has been reported to be associated with tumor development and progression as well as to protect cells from apoptosis induced by various cellular stresses. Through a tetracycline-regulated COX-2 overexpression system, we found that COX-2 inhibits detachment-induced apoptosis (anoikis) in a human bladder cancer cell line, EJ. We also found that the inhibition of anoikis by COX-2 results from activation of the PI-3K/Akt pathway as evidenced by suppression of the COX-2 effect on anoikis by a PI-3K inhibitor, LY294002. Furthermore, COX-2 enhanced Mcl-1 expression in the anoikis process, implying that Mcl-1 also may be involved in mediating the survival function of COX-2. Together, these results suggest that COX-2 inhibits anoikis by activation of the PI-3K/Akt pathway and probably by enhancement of Mcl-1 expression in human bladder cancer cells. This anti- anoikis effect of COX-2 may be a part of mechanisms to promote tumor development and progression.

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Affiliations

  1. Department of Biochemistry and Molecular Biology, Kangwon National University College of Medicine, Chuncheon, 200-701, Korea

    Eun-Mi Choi

Authors
  1. Eun-Mi Choi
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  2. Sahng-June Kwak
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  3. Young-Myeong Kim
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  4. Kwon-Soo Ha
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  5. Jong-Il Kim
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  6. Sam W Lee
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  7. Jeong A Han
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This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Choi, EM., Kwak, SJ., Kim, YM. et al. COX-2 inhibits anoikis by activation of the PI-3K/Akt pathway in human bladder cancer cells. Exp Mol Med 37, 199–203 (2005). https://doi.org/10.1038/emm.2005.27

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Keywords

  • anoikis
  • bladder
  • cancer
  • COX-2
  • Mcl-1
  • PI-3K/Akt

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