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首页> 外文期刊>Cell biology international. >Inhibition of invasiveness of human lung cancer cell line H1299 by over-expression of cofilin.
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Inhibition of invasiveness of human lung cancer cell line H1299 by over-expression of cofilin.

机译：过表达cofilin抑制人肺癌细胞H1299侵袭性。

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The Rho-LIM-kinase (LIMK) signaling pathway, believed to be involved in the regulation of tumor invasion, specifically regulates the activity of cofilin. However, it is unclear whether cofilin plays a pivotal role in tumor invasiveness. In this paper we show using a tet-on gene expression system that over-expression of cofilin inhibits the invasiveness of human lung cancer H1299 cells. Over-expressed cofilin disrupts the actin cytoskeleton at the leading edge of the cell and up-regulates p27(kip1), which is known to be involved in regulating cell motility. Removal of cofilin over-expression normalizes the p27(kip1) level and concomitantly restores the invasiveness of the cultured cells. These findings suggest that excessive cofilin production might prevent cancer cell invasion.
机译：Rho-LIM激酶（LIMK）信号通路被认为与肿瘤侵袭的调节有关，它专门调节cofilin的活性。然而，尚不清楚cofilin在肿瘤侵袭性中是否起关键作用。在本文中，我们显示了使用tet-on基因表达系统，cofilin的过表达抑制了人类肺癌H1299细胞的侵袭性。过表达的cofilin破坏了细胞前沿的肌动蛋白细胞骨架，并上调了p27（kip1），已知该蛋白与调节细胞运动有关。去除cofilin的过表达可使p27（kip1）水平正常化，并同时恢复培养细胞的侵袭性。这些发现表明，过多的丝素蛋白产生可能阻止癌细胞的侵袭。

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