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首页> 美国卫生研究院文献>British Journal of Cancer >Hypoxia facilitates tumour cell detachment by reducing expression of surface adhesion molecules and adhesion to extracellular matrices without loss of cell viability.
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Hypoxia facilitates tumour cell detachment by reducing expression of surface adhesion molecules and adhesion to extracellular matrices without loss of cell viability.

机译：缺氧通过减少表面粘附分子的表达和对细胞外基质的粘附而促进肿瘤细胞的分离而不会损失细胞的活力。

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摘要

The effects of acute hypoxia on integrin expression and adhesion to extracellular matrix proteins were investigated in two human melanoma cell lines, HMB-2 and DX3, and a human adenocarcinoma cell line, HT29. Exposure to hypoxia caused a significant down-regulation of cell surface integrins and an associated decrease in cell adhesion. Loss of cell adhesion and integrin expression were transient and levels returned to normal within 24 h of reoxygenation. Other cell adhesion molecules, such as CD44 and N-CAM, were also down-regulated after exposure of cells to hypoxia. Acute exposure to hypoxia of cells at confluence caused rapid cell detachment. Cell detachment preceded loss of viability. Detached HMB-2 and DX3 cells completely recovered upon reoxygenation, and floating cells re-attached and continued to grow irrespective of whether they were left in the original glass dishes or transferred to new culture vessels, while detached HT29 cells partly recovered upon reoxygenation. Cell detachment after decreased adhesion appears to be a stress response, which may be a factor enabling malignant cells to escape hypoxia in vivo, with the potential to form new foci of tumour growth.
机译：在两个人类黑素瘤细胞系HMB-2和DX3和一个人类腺癌细胞系HT29中研究了急性缺氧对整联蛋白表达和粘附于细胞外基质蛋白的影响。暴露于缺氧状态会导致细胞表面整联蛋白显着下调，并导致细胞粘附性降低。细胞粘附和整联蛋白表达的丧失是短暂的，并且在复氧后24小时内水平恢复正常。细胞暴露于缺氧后，其他细胞粘附分子（例如CD44和N-CAM）也被下调。汇合处细胞缺氧的急性暴露导致细胞快速脱离。细胞脱落先于活力丧失。分离的HMB-2和DX3细胞在重新充氧后完全恢复，并且漂浮细胞重新附着并继续生长，无论它们是否留在原始玻璃皿中或转移到新的培养皿中，而分离的HT29细胞在重新充氧后部分恢复。粘附力降低后的细胞脱离似乎是应激反应，这可能是使恶性细胞在体内逃脱缺氧的一个因素，有可能形成新的肿瘤生长灶。

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