Cytoplasmic dye transfer between metastatic tumor cells and vascular endothelium.
Cytoplasmic dye transfer between metastatic tumor cells and vascular endothelium.
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DOI：
10.1083/jcb.115.5.1375
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发表时间：
1991-12
影响因子：
7.8
通讯作者：
Pauli, B U
中科院分区：
文献类型：
--
作者：
el-Sabban, M E;Pauli, B U
继发性器官部位的转移性定植是通过血液传播的肿瘤细胞附着于微血管内皮细胞表面表达的器官特异性粘附分子而启动的。使用数字视频成像显微镜和荧光激活细胞分选技术，我们在这里显示，高转移性细胞（B16-F10小鼠黑色素瘤和R3230 AC-MET大鼠乳腺癌细胞）先前标记的荧光染料BCECF开始转移染料内皮细胞单层后不久，建立粘附。BCECF转移到内皮细胞单层的程度取决于接种到内皮细胞单层上的BCECF标记的肿瘤细胞的数量和两种细胞类型的共培养时间，如通过内皮细胞特异性mAb染色的细胞中BCECF阳性细胞数量的增加所观察到的。随着共培养时间的延长，BCECF标记的肿瘤细胞群的荧光强度逐渐减弱，染料转移到BAEC单层。染料的转移是双向的，并对1-庚醇的抑制敏感。相反，转移性差的B16-F0黑色素瘤细胞和非转移性R3230 AC-LR乳腺癌细胞不能有效地与血管内皮细胞偶联。从这些实验和肿瘤细胞表达的连接蛋白43 mRNA的量推断，肿瘤细胞/内皮细胞通信是由间隙连接通道介导的，并且这种相互作用可能在继发部位的肿瘤细胞外渗中起关键作用。
Metastatic colonization of a secondary organ site is initiated by the attachment of blood-borne tumor cells to organ-specific adhesion molecules expressed on the surface of microvascular endothelial cells. Using digital video imaging microscopy and fluorescence activated cell sorting techniques, we show here that highly metastatic cells (B16-F10 murine melanoma and R3230AC-MET rat mammary adenocarcinoma cells) previously labeled with the fluorescent dye BCECF begin to transfer dye to endothelial cell monolayers shortly after adhesion is established. The extent of BCECF transfer to endothelial cell monolayers is dependent upon the number of BCECF-labeled tumor cells seeded onto the endothelial cell monolayer and the time of coculture of the two cell types, as visualized by an increase in the number of BCECF-positive cells among cells stained with an endothelial cell-specific mAb. Dye transfer to BAEC monolayers proceeds with a progressive loss of fluorescence intensity in the BCECF-labeled tumor cell population with time of coculture. The transfer of dye is bidirectional and sensitive to inhibition by 1-heptanol. In contrast, poorly metastatic B16-F0 melanoma cells and non-metastatic R3230AC-LR mammary adenocarcinoma cells do not efficiently couple with vascular endothelial cells. It is inferred from these experiments and from the amounts of connexin43 mRNA expressed by tumor cells that tumor cell/endothelial cell communication is mediated by gap junctional channels and that this interaction may play a critical role in tumor cell extravasation at secondary sites.