Effect of pro-inflammatory stimuli on tumor cell-mediated induction of endothelial cell adhesion molecules in vitro.
The object of our study was the question about the relevance of the tumor surrounding inflammatory cells with respect to the metastatic potential of the tumor cells. To imitate the role of inflammatory cells, three colon carcinoma (HT-29, HRT-18, and SW-620), one breast carcinoma (MCF-7), and one melanoma (ST-ML-12) cell lines were treated with pro-inflammatory stimuli, LPS, TNF-alpha, or IL-1beta. HUVEC monolayers were then stimulated by the collected supernatants (SN) of the tumor cells, following washing out of the applied stimuli. Analysis of CAM expression on HUVEC was performed using cell enzyme immunoassay. E-selectin, VCAM-1, and, in part, ICAM-1 were significantly up-regulated on HUVEC by exposure to SN of all LPS-stimulated tumor cells. This was especially the case for the colon carcinoma cell lines. A minimal increase of expression of VCAM-1 was observed after exposure to SN from TNF-alpha-stimulated HT-29 and MCF-7 cells. IL-1beta stimulation had no effect on endothelial CAM expression. These observations indicate that LPS could play a crucial role in tumor metastasis by inducing the release of soluble factors from different tumor cell lines capable of up-regulating CAM expression. This might be of special significance in colon carcinomas, where a large source of bacterial LPS is available in the intestinal lumen.
Institute of Pathology, Johannes Gutenberg University, Mainz, Germany.
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Simiantonaki
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Jayasinghe
C J
CJ
Kirkpatrick
D001943:Breast Neoplasms / Q000188:drug therapy / Q000378:metabolism; D002277:Carcinoma / Q000188:drug therapy / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000032:analysis / Q000096:biosynthesis*; D002478:Cells, Cultured; D003110:Colonic Neoplasms / Q000188:drug therapy / Q000378:metabolism; D017077:Culture Media, Conditioned / Q000494:pharmacology; D019040:E-Selectin / Q000032:analysis / Q000096:biosynthesis; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D007249:Inflammation / Q000276:immunology / Q000378:metabolism*; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000096:biosynthesis; D007375:Interleukin-1 / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008545:Melanoma / Q000188:drug therapy / Q000378:metabolism; D009369:Neoplasms / Q000188:drug therapy / Q000378:metabolism*; D014407:Tumor Cells, Cultured; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*; D015854:Up-Regulation / Q000187:drug effects; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis / Q000096:biosynthesis
D015815:Cell Adhesion Molecules; D017077:Culture Media, Conditioned; D019040:E-Selectin; D007375:Interleukin-1; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1