Up‐regulation of intercellular adhesion molecule 1 (ICAM‐1) on human renal cell carcinoma cells by interleukin‐4
- 29 May 1995
- journal article
- research article
- Published by Wiley in International Journal of Cancer
- Vol. 61 (5) , 635-642
- https://doi.org/10.1002/ijc.2910610509
Abstract
We have previously demonstrated that human renal cell carcinoma (RCC) cells express high‐affinity IL‐4 receptors (IL‐4R). To study the functions of these receptors, we have examined the effect of IL‐4 on the expression of intercellular adhesion molecule‐1 (ICAM‐1 or CD54) on human RCC cells. Following incubation with various concentrations of IL‐4, RCC cells were examined for ICAM‐1 expression by flow cytometric analysis. The 2 primary RCC cell cultures and the 2 cell lines examined expressed varying basal levels of ICAM‐1 on the cell surface. IL‐4 treatment increased ICAM‐1 expression in a time‐dependent manner and maximum augmentation of ICAM‐1 expression was observed after a 48 hr incubation. The increase in ICAM‐1 expression was specific because anti‐hIL‐4 antibody blocked this effect. No enhancement of ICAM‐1 expression was observed when RCC cells were incubated with IL‐4 in the presence of cycloheximide, indicating that the IL‐4 effect requires new protein synthesis. Up‐regulation of ICAM‐1 expression was also observed at the mRNA level and maximum increase in message occurred 8 hr post‐IL‐4 treatment. Both IL‐4 and IFN‐γ also increased soluble ICAM‐1 levels in WS‐RCC culture supernatant. The significance of enhanced soluble and surface ICAM‐1 expression was investigated by examining the lymphokine activated killer (LAK) cell‐mediated lysis of IL‐4‐treated WS‐RCC cells. LAK cells lysed WS‐RCC cells very effectively, but lysis observed in target cells pre‐treated with IL‐4 did not correlate with the increased expression of ICAM‐1 antigen. Our results indicate a previously unknown function of IL‐4 on RCC and further demonstrate that IL‐4R on RCC are functional. © 1995 Wiley‐Liss, Inc.Keywords
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