Heat shock and cytokines modulate the expression of adhesion molecules on different human gastric-cancer cell lines

Mao-Chih Hsieh, C. W. Wu, L. H. Wu, W. Y. Lui, F. K. P'eng, C. L. Yu

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)

Abstract

In order to understand the expression and modulation of adhesion molecules (AMs) on the surface of different gastric cancers, we studied 4 gastric-cancer cell lines including SC-M1, KATO-III, AGS and AZ-521. The expression of E-cadherin, integrins (β1, β2 and β3), ICAMs (1 and 2), and CD11 (a, b and c) on the cells was detected by flow cytometry. We found that E-cadherin was only expressed on SC-M1 and KATO-III. CD29 (β1 integrin) could be found in cells of all 4 lines. CD54 (ICAM-1) could not be detected in AZ-521. In contrast, CD18 (β2 integrin), CD61 (β3 integrin), ICAM-2, CD11a, CD11b and CD11c were all absent from these cells. Heat-shock treatment (42.5°C, 60 min) enhanced the expression of E-cadherin, CD29 and CD54 on SC-M1, and of CD29 on AGS. In addition, TNF-α (50 U/ml) and IL-1β (10 U/ml) modulated the expression of these AMs,like heat-shock treatment. The increment of these adhesion molecules caused by heat shock, TNF-α and IL-1β stimulation on SC-M1 was also confirmed by Western blot analysis. Functionally, these treatments increased the binding between normal human mononuclear cells and SC-M1 cells. The heat-shock treatment could induce a significant amount of TNF-α and IL-1β release from SC-M1 and KATO-III, but seemed irrelevant to the expression of AMs. These results suggest that limited adhesion molecules were expressed on the surface of different gastric cancer cells. Heat shock, IL-1β and TNF-α may selectively modulate the expression of these 3 molecules on some of the cells, and this is probably related to their antitumor effect.

Original languageEnglish
Pages (from-to)690-694
Number of pages5
JournalInternational Journal of Cancer
Volume67
Issue number5
DOIs
Publication statusPublished - Sep 23 1996
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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