Overexpression of IL-1ra gene up-regulates interleukin-1β converting enzyme (ICE) gene expression: Possible mechanism underlying IL-1β-resistance of cancer cells View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1999-08-27

AUTHORS

M Sumitomo, M Tachibana, M Murai, M Hayakawa, H Nakamura, A Takayanagi, N Shimizu

ABSTRACT

We investigated the interaction of endogenous interleukin (IL)-1β, IL-1ra, and interleukin-1β converting enzyme (ICE) in four human urological cancer cell lines, KU-19-19, KU-1, KU-2 and KU-19-20. Northern blot analysis showed that IL-1β gene was expressed in all cell lines. On the other hand, in KU-19-19 and KU-19-20, the gene expressions of both IL-1ra and ICE were suppressed. MTT assay revealed that IL-1β (10 ng ml–1) promoted cell growth in KU-19-19 and KU-19-20, while it inhibited in KU-1 and KU-2. An ICE inhibitor, Acetyl-Tyr-Val-Ala-Asp-CHO (YVAD-CHO) blocked IL-1β-induced growth inhibition in KU-1 and KU-2. Overexpression of the secretory type IL-1ra with adenovirus vector (AxIL-1ra) enhanced ICE gene expression, while exogenous IL-1ra (100 ng ml–1) did not enhance it. Furthermore, AxIL-1ra treatment promoted endogenous IL-1β secretion and induced significant growth inhibition and apoptotic cell death on KU-19-19 and KU-19-20. Treatment with either IL-1ra (100 ng ml–1), IL-1β antibody (100 μg ml–1), or YVAD-CHO blocked AxIL-1ra-induced cell death in KU-19-19 and KU-19-20. These results suggest that IL-1β-sensitivity depends on the level of ICE gene expression, which is regulated by the level of endogenous sIL-1ra expression. This is a first report on the intracellular function of sIL-1ra and these findings may provide key insights into the mechanism underlying the viability of cancer cells. More... »

PAGES

277-286

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.bjc.6690688

DOI

http://dx.doi.org/10.1038/sj.bjc.6690688

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1002768322

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/10496353


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