HEAT-SHOCK AND CYTOKINES MODULATE THE EXPRESSION OF ADHESION MOLECULES ON DIFFERENT HUMAN GASTRIC-CANCER CELL-LINES

In order to understand the expression and modulation of adhesion molec ules (AMs) on the surface of different gastric cancers, we studied 4 g astric-cancer cell lines including SC-MI, KATO-III, AGS and AZ-521. Th e expression of E-cadherin, integrins (beta 1, beta 2 and beta 3), ICA Ms(1 and 2), and CD11 (a, b and c) on the cells was detected by flow c ytometry. We found that E-cadherin was only expressed on SC-MI and KAT O-III. CD29 (beta 1 integrin) could be found in cells of all 4 lines. CD54 (ICAM-I) could not be detected in AZ-521. In contrast, CD18 (beta 2 integrin), CD61 (beta 3 integrin), ICAM-2, CD11a, CD11b and CD I Ic were all absent from these cells. Heat-shock treatment (42.5 degrees C, 60 min) enhanced the expression of E-cadherin, CD29 and CD54 on SC- M I, and of CD29 on AGS. In addition, TNF-alpha (50U/ml) and IL-I beta (10U/ml) modulated the expression of these AMs, like heat-shock treat ment. The increment of these adhesion molecules caused by heat shock, TNF-alpha and IL-I beta stimulation on SC-MI was also confirmed by Wes tern blot analysis. Functionally, these treatments increased the bindi ng between normal human mononuclear cells and SC-MI cells. The heat-sh ock treatment could induce a significant amount of TNF-alpha and IL-1 beta release from SC-MI and KATO-III, but seemed irrelevant to the exp ression of AMs. These results suggest that limited adhesion molecules were expressed on the surface of different gastric cancer cells. Heat shock, IL-1 beta and TNF-alpha may selectively modulate the expression of these 3 molecules on some of the cells, and this is probably relat ed to their antitumor effect. (C) 1996 Wiley-Liss, Inc.