Influence of proinflammatory cytokines on the adhesion of human colon carcinoma cells to lung microvascular endothelium
(c) 2004 Wiley-Liss, Inc..
In this experimental study, the influence of surgery-induced proinflammatory cytokines on tumor recurrence in the lung was investigated. A reproducible human in vitro assay was developed to study the adhesion of HT29 colon carcinoma cells to monolayers of microvascular endothelial cells of the lung (HMVECs-L) or human umbilical venous endothelial cells (HUVECs). Preincubation of HMVECs-L with maximally active concentrations of IL-1beta and TNF-alpha, but not with IL-6, resulted in at least 250% adhesion compared to control adhesion (p <or= 0.01). The effect of IL-1beta and TNF-alpha was concentration- and time-dependent. Comparable results were found for HUVECs. Tumor cell adhesion was not increased after preincubation of HT29 with TNF-alpha. Enzyme immunoassays of cytokine-preincubated HUVECs and HMVECs-L showed concentration- and time-dependent upregulation of E-selectin, ICAM-1 and VCAM-1 expression. In addition, LFA-1 and VLA-4 were only expressed on HMVECs-L, creating more binding possibilities for HMVECs-L compared to HUVECs. Inhibition assays with anti-E-selectin monoclonal antibody significantly decreased tumor cell adhesion to HUVECs; however, it did not affect tumor cell adhesion to HMVECs-L. Furthermore, anti-ICAM-1 and anti-VCAM-1 antibodies did not affect adhesion. Our results prove IL-1beta and TNF-alpha promote tumor cell adhesion to HMVECs-L in vitro and may therefore account for enhanced tumor recurrence in the lung seen after major surgical trauma. The adhesion of HT29 to HUVEC is inhibitable by E-selectin antibodies, whereas the adhesion to HMVEC-L is not inhibitable by these antibodies. Probably not one but a complex of adhesion molecules is responsible for enhanced adhesion to HMVECs-L.
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
2004 |
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| Erschienen: |
2004 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:112 |
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| Enthalten in: |
International journal of cancer - 112(2004), 6 vom: 20. Dez., Seite 943-50 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
ten Kate, Miranda [VerfasserIn] |
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| Anmerkungen: |
Date Completed 30.11.2004 Date Revised 03.03.2016 published: Print Citation Status MEDLINE |
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| Förderinstitution / Projekttitel: |
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NLM150604076 |
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| 100 | 1 | |a ten Kate, Miranda |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Influence of proinflammatory cytokines on the adhesion of human colon carcinoma cells to lung microvascular endothelium |
| 264 | 1 | |c 2004 | |
| 336 | |a Text |b txt |2 rdacontent | ||
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| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a (c) 2004 Wiley-Liss, Inc. | ||
| 520 | |a In this experimental study, the influence of surgery-induced proinflammatory cytokines on tumor recurrence in the lung was investigated. A reproducible human in vitro assay was developed to study the adhesion of HT29 colon carcinoma cells to monolayers of microvascular endothelial cells of the lung (HMVECs-L) or human umbilical venous endothelial cells (HUVECs). Preincubation of HMVECs-L with maximally active concentrations of IL-1beta and TNF-alpha, but not with IL-6, resulted in at least 250% adhesion compared to control adhesion (p <or= 0.01). The effect of IL-1beta and TNF-alpha was concentration- and time-dependent. Comparable results were found for HUVECs. Tumor cell adhesion was not increased after preincubation of HT29 with TNF-alpha. Enzyme immunoassays of cytokine-preincubated HUVECs and HMVECs-L showed concentration- and time-dependent upregulation of E-selectin, ICAM-1 and VCAM-1 expression. In addition, LFA-1 and VLA-4 were only expressed on HMVECs-L, creating more binding possibilities for HMVECs-L compared to HUVECs. Inhibition assays with anti-E-selectin monoclonal antibody significantly decreased tumor cell adhesion to HUVECs; however, it did not affect tumor cell adhesion to HMVECs-L. Furthermore, anti-ICAM-1 and anti-VCAM-1 antibodies did not affect adhesion. Our results prove IL-1beta and TNF-alpha promote tumor cell adhesion to HMVECs-L in vitro and may therefore account for enhanced tumor recurrence in the lung seen after major surgical trauma. The adhesion of HT29 to HUVEC is inhibitable by E-selectin antibodies, whereas the adhesion to HMVEC-L is not inhibitable by these antibodies. Probably not one but a complex of adhesion molecules is responsible for enhanced adhesion to HMVECs-L | ||
| 650 | 4 | |a Journal Article | |
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| 700 | 1 | |a Hofland, Leo J |e verfasserin |4 aut | |
| 700 | 1 | |a van Grevenstein, Wilhelmina M U |e verfasserin |4 aut | |
| 700 | 1 | |a van Koetsveld, Peter V |e verfasserin |4 aut | |
| 700 | 1 | |a Jeekel, Johannes |e verfasserin |4 aut | |
| 700 | 1 | |a van Eijck, Casper H J |e verfasserin |4 aut | |
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