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首页> 外文期刊>Cellular Physiology and Biochemistry >K(+) channel-dependent migration of fibroblasts and human melanoma cells.
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K(+) channel-dependent migration of fibroblasts and human melanoma cells.

机译：K（+）通道依赖的成纤维细胞和人类黑色素瘤细胞迁移。

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摘要

Previously, we showed that migration of transformed renal epithelial cells (MDCK-F cells) is a K(+) channel-dependent process [J Clin Invest 1994;93:1631]. In order to determine whether K(+) channel activity is a general requirement for locomotion, we extended our observations to NIH3T3 fibroblasts and human melanoma cells. Migration of both cell types and its dependence on K(+) channel activity was measured at the single cell level by time lapse photography in the absence and presence of the specific K(+) channel blocker charybdotoxin (CTX). Locomotion of both cell types is inhibited by K(+) channel blockade. CTX slows down migration of fibroblasts and of melanoma cells dose-dependently by up to 61 +/- 11%. These findings suggest that K(+) channel activity is a general prerequisite for migration. To determine whether CTX-induced inhibition of migration of fibroblasts and melanoma cells involves quantitative changes of actin filaments, we indirectly measured filamentous actin by quantitating binding of fluorescently labeled phalloidin. Whereas CTX elicits a decrease of bound phalloidin in fibroblasts there is an increase in melanoma cells. Since migration of tumor cells is required for invading surrounding tissue, we developed an assay to test whether CTX-induced inhibition of migration also impairs invasion of melanoma cells. Melanoma cells were seeded on a layer of high resistance renal epithelial cells (MDCK cells clone C7; transepithelial resistance R(te) >3,000 Omegacm(2)) and R(te) was measured daily. R(te) starts to decrease 2 days after seeding of melanoma cells onto MDCK-C7 cells. By day 7, R(te) has dropped to 24 +/- 1.5% of control. K(+) channel blockade with CTX (10 nmol/l) cannot prevent or delay this drop of R(te). R(te) reaches the same level with or without CTX. These results indicate that the disruption of an epithelial layer, unlike migration of melanoma cells, cannot be modulated by K(+) channel blockade.
机译：以前，我们证明了转化的肾上皮细胞（MDCK-F细胞）的迁移是K（+）通道依赖性过程[J Clin Invest 1994; 93：1631]。为了确定K（+）通道的活动是否是运动的一般要求，我们将观察范围扩展到NIH3T3成纤维细胞和人类黑色素瘤细胞。两种细胞类型的迁移及其对K（+）通道活性的依赖性是通过在不存在和存在特定K（+）通道阻断剂charybdotoxin（CTX）的情况下通过延时摄影在单个细胞水平上进行测量的。两种细胞类型的运动都受到K（+）通道阻滞的抑制。 CTX剂量依赖性地使成纤维细胞和黑色素瘤细胞的迁移减慢多达61 +/- 11％。这些发现表明K（+）通道活动是迁移的一般前提。为了确定CTX诱导的成纤维细胞和黑色素瘤细胞迁移抑制是否涉及肌动蛋白丝的定量变化，我们通过定量荧光标记的鬼笔环肽的结合来间接测量丝状肌动蛋白。 CTX引起成纤维细胞中结合的鬼笔环肽减少，而黑色素瘤细胞增加。由于侵袭周围组织需要肿瘤细胞的迁移，因此我们开发了一种测定法来测试CTX诱导的迁移抑制是否也损害黑素瘤细胞的侵袭。将黑素瘤细胞接种在一层高抗性肾上皮细胞（MDCK细胞克隆C7;经上皮抗性R（te）> 3,000 Omegacm（2））上，并每天测量R（te）。黑素瘤细胞接种到MDCK-C7细胞后2天，R（te）开始下降。到第7天，R（te）已降至对照的24 +/- 1.5％。使用CTX（10 nmol / l）的K（+）通道封锁不能阻止或延迟R（te）的下降。不管有没有CTX，R（te）都达到相同的水平。这些结果表明，与黑色素瘤细胞的迁移不同，上皮层的破坏不能通过K（+）通道阻滞来调节。

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