Open Access

‘Decoy’ and ‘non-decoy’ functions of DcR3 promote malignant potential in human malignant fibrous histiocytoma cells

  • Authors:
    • Mitsunori Toda
    • Teruya Kawamoto
    • Takeshi Ueha
    • Kenta Kishimoto
    • Hitomi Hara
    • Naomasa Fukase
    • Yasuo Onishi
    • Risa Harada
    • Masaya Minoda
    • Masahiro Kurosaka
    • Toshihiro Akisue
  • View Affiliations

  • Published online on: June 28, 2013     https://doi.org/10.3892/ijo.2013.1999
  • Pages: 703-712
  • Copyright: © Toda et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

Decoy receptor 3 (DcR3) is a soluble secreted protein that belongs to the tumor necrosis factor receptor (TNFR) superfamily. DcR3 inhibits the Fas ligand (FasL)/Fas apoptotic pathway by binding to FasL, competitively with Fas receptor. Previous studies have reported that overexpression of DcR3 has been detected in various human malignancies and that DcR3 functions as a ‘decoy’ for FasL to inhibit FasL-induced apoptosis. In addition, recent studies have revealed that DcR3 has ‘non-decoy’ functions to promote tumor cell migration and invasion, suggesting that DcR3 may play important roles in tumor progression by decoy and non-decoy functions. We have previously reported that overexpression of DcR3 was observed in human malignant fibrous histiocytoma (MFH), however, the roles of DcR3 in MFH have not been studied. In the present study, to elucidate the roles of DcR3 in tumor progression of MFH, we examined the effects of DcR3 inhibition on cell apoptosis, migration and invasion in human MFH cells. siRNA knockdown of DcR3 enhanced the FasL-induced apoptotic activity and significantly decreased cell migration and invasion with a decrease in the activation of phosphatidylinositol 3 kinase (PI3K)/Akt and matrix metalloproteinase (MMP)-2. The findings in this study strongly suggest that DcR3 plays important roles in tumor progression of human MFH by decoy as well as non-decoy functions and that DcR3 may serve as a potent therapeutic target for human MFH.
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September 2013
Volume 43 Issue 3

Print ISSN: 1019-6439
Online ISSN:1791-2423

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Spandidos Publications style
Toda M, Kawamoto T, Ueha T, Kishimoto K, Hara H, Fukase N, Onishi Y, Harada R, Minoda M, Kurosaka M, Kurosaka M, et al: ‘Decoy’ and ‘non-decoy’ functions of DcR3 promote malignant potential in human malignant fibrous histiocytoma cells. Int J Oncol 43: 703-712, 2013
APA
Toda, M., Kawamoto, T., Ueha, T., Kishimoto, K., Hara, H., Fukase, N. ... Akisue, T. (2013). ‘Decoy’ and ‘non-decoy’ functions of DcR3 promote malignant potential in human malignant fibrous histiocytoma cells. International Journal of Oncology, 43, 703-712. https://doi.org/10.3892/ijo.2013.1999
MLA
Toda, M., Kawamoto, T., Ueha, T., Kishimoto, K., Hara, H., Fukase, N., Onishi, Y., Harada, R., Minoda, M., Kurosaka, M., Akisue, T."‘Decoy’ and ‘non-decoy’ functions of DcR3 promote malignant potential in human malignant fibrous histiocytoma cells". International Journal of Oncology 43.3 (2013): 703-712.
Chicago
Toda, M., Kawamoto, T., Ueha, T., Kishimoto, K., Hara, H., Fukase, N., Onishi, Y., Harada, R., Minoda, M., Kurosaka, M., Akisue, T."‘Decoy’ and ‘non-decoy’ functions of DcR3 promote malignant potential in human malignant fibrous histiocytoma cells". International Journal of Oncology 43, no. 3 (2013): 703-712. https://doi.org/10.3892/ijo.2013.1999