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[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

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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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What this paper is about

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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Available 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.

Key concepts: Vitronectin, Fibronectin, Extracellular matrix, Integrin, Laminin, Adhesion, Cell adhesion, Cell adhesion molecule

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[Different integrin-induced adhesion of highly liver metastatic and little metastatic colon carcinoma cells in an extracellular matrix]. — Research Paper | ScholarLens