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Title 

Up-regulation of reactive oxygen species(ROS) and resistance to Fas-mediated apoptosis in the C33A cervical cancer cell line transfected with IL-18 receptor

Authors 

Do Young YoonYoung Sik ChoJ W ParkS H KimJ W Kim

Publisher 

Walter de Gruyter

Issue Date 

2004

Citation 

Clinical Chemistry and Laboratory Medicine, vol. 42, no. 5, pp. 499-506

Keywords 

FasFas ligandIL-18IL-18 receptorreactive oxygen species (ROS)cell adhesion moleculeFas antibodyFas antigenFAS ligandintercellular adhesion molecule 1

Abstract 

Cervical cancer cells were transfected with a newly discovered interleukin (IL)-18 receptor to investigate the effect of endogenous IL-18 on the regulation of immune-related factors such as Fas (CD95/Apo-1)/Fas ligand and intercellular adhesion molecules. Transfection of the IL-18 receptor selectively induced a slight enhancement of the Fas via the up-regulation of intracellular reactive oxygen species and IL-18 in cervical carcinoma C33A cells, whereas there were no effects on the expression of p53, intercellular adhesion molecules-1 and Fas ligand. Neither IL-18 receptor transfection nor recombinant IL-18 enhanced interferon-γ production in C33A cells. Thus, IL-18 receptor transfection induced IL-18 expression and enhanced intracellular reactive oxygen species and Fas expression in C33A cells in an interferon-γ-independent pathway. However, treatment with agonistic anti-Fas antibody did not induce the apoptosis of C33A/IL-18 receptor transfectants, suggesting that either reactive oxygen species play a key role in resisting the Fas-induced apoptosis of C33A cells, or Fas was not functional. These results show that C33A/IL-18 receptor cells are resistant to the apoptosis and thus can survive against the immune surveillance and activated immune cells. Our results thus suggest that IL-18 and IL-18 receptor, together, may play a role in immunoregulation or in inflammation by augmenting the levels of IL-18 and reactive oxygen species in C33A cells.

ISSN 

1434-6621

Link 

http://dx.doi.org/10.1515/CCLM.2004.085

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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