Signal transduction system responsible for the retraction of vascular endothelial cells upon cancer cell invasion or metastasis

这是众所周知的，因为VEC完整性的损失在生理学或病理学现象中的关键作用，例如炎症或癌症metastasis。在这一研究中，我们研究了细胞系离子化Ca 2+ （[Ca 2 +]i）中的VEC还原诱导。vEC激活模式是通过直接细胞对细胞接触或癌症细胞秘密的溶解因子被单独分析的。使用Ca 2+指示器、荧光-3、清晰演示[Ca 2 +]在人类遮蔽性血管内（HUVECs）上与人类乳腺癌细胞线（MCF-7）上细胞接触的数字成像分析，但未被外切拉尔Ni 2+抑制，被预处理细胞。Although培养介质也从MCF-7中提取出VEC提取作为一个好的[Ca 2 +]i吸收，原材料被抑制了对该培养介质的热处理，建议[Ca 2 +]碘提取不是VEC提取的必要条件。

It is well known that the loss of VEC integrity plays pivotal roles in several physiological or pathological phenomena, such as inflammation or cancer metastasis. In this study, we studied the possible involvement of cytoplasmic ionized Ca2+ ([Ca2+]i) in VEC retraction induced by cancer cells. The mode of vEC activation by direct cell-to-cell contact or cancer cell secreted soluble factors was separately analyzed. Digital imaging analysis using Ca2+ indicator, fluo-3, cleary demonstrated [Ca2+]i oscillation in human umbilical vein endothelial cells (HUVECs) upon cell contact with human breast cancer cell line, MCF-7, which was not inhibited by extracellular Ni2+ and was inhibited by pretreating the cells by paraformaldehyde. Although culture medium derived from MCF-7 also caused VEC retraction aァ well as [Ca2+]i oscillation, the former was inhibited by the heat-treatment of the culture medium, suggesting that [Ca2+]i osillation is not essential in VEC retraction induced by cancer derived soluble factors.