[Different integrin-induced adhesion of highly liver metastatic and little metastatic colon carcinoma cells in an extracellular matrix].
Jörg Haier, Marwan Y. Nasralla, HJ Buhr, Nicolson Gl
Abstract
Jörg Haier, Marwan Y. Nasralla, HJ Buhr, Nicolson Gl
Abstract
Poorly and highly liver metastatic colon carcinoma cell lines have different integrin-mediated adhesion to extracellular matrix. Specific integrin-mediated interactions between tumor cells and extracellular matrix (ECM) in the host organs are important for organ-specific metastasis. In colon carcinoma integrin expression differs depending on the metastatic potential of the tumor. Integrin-mediated adhesion of poorly (HT-29P) and highly liver-metastatic (HT-29LMM) colon carcinoma to extracellular matrix (ECM; Collagen I-C I, Collagen IV-C IV, Laminin LN, Fibronectin FN, Vitronectin VN) was investigated. HT-29LMM showed significant better adhesion to LN (45% vs. 26%; p < 0.001) and FN 20% vs. 1%; p < 0.001). No adhesion was found to VN. RGD-oligopeptides completely inhibited adhesion to FN. Using inhibition with anti-integrin-mAB it was shown, that adhesion to C I and C IV is mediated by alpha 2 beta 1-integrin, adhesion to LN by alpha 6 beta 1 and adhesion to FN by alpha v beta 1. These results have shown that adhesion of HT-29 cells is mediated by different integrins depending on ECM components. Poorly and highly metastatic cells possessed different patterns of adhesion to various substrates.
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Poorly and highly liver metastatic colon carcinoma cell lines have different integrin-mediated adhesion to extracellular matrix. Specific integrin-mediated interactions between tumor cells and extracellular matrix (ECM) in the host organs are important for organ-specific metastasis. In colon carcinoma integrin expression differs depending on the metastatic potential of the tumor. Integrin-mediated adhesion of poorly (HT-29P) and highly liver-metastatic (HT-29LMM) colon carcinoma to extracellular matrix (ECM; Collagen I-C I, Collagen IV-C IV, Laminin LN, Fibronectin FN, Vitronectin VN) was investigated. HT-29LMM showed significant better adhesion to LN (45% vs. 26%; p < 0.001) and FN 20% vs. 1%; p < 0.001). No adhesion was found to VN. RGD-oligopeptides completely inhibited adhesion to FN. Using inhibition with anti-integrin-mAB it was shown, that adhesion to C I and C IV is mediated by alpha 2 beta 1-integrin, adhesion to LN by alpha 6 beta 1 and adhesion to FN by alpha v beta 1. These results have shown that adhesion of HT-29 cells is mediated by different integrins depending on ECM components. Poorly and highly metastatic cells possessed different patterns of adhesion to various substrates.
Key concepts: Vitronectin, Fibronectin, Extracellular matrix, Integrin, Laminin, Adhesion, Cell adhesion, Cell adhesion molecule