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首页> 外文期刊>Cell and Tissue Research >A novel role of ribonuclease inhibitor in regulation of epithelial-to-mesenchymal transition and ILK signaling pathway in bladder cancer cells
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A novel role of ribonuclease inhibitor in regulation of epithelial-to-mesenchymal transition and ILK signaling pathway in bladder cancer cells

机译：核糖核酸酶抑制剂在膀胱癌细胞上皮-间充质转化和ILK信号通路调控中的新作用

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摘要

Human ribonuclease inhibitor (RI) is a cytoplasmic acidic protein possibly involved in biological functions other than the inhibition of RNase A and angiogenin activities. We have previously shown that RI can inhibit growth and metastasis in some cancer cells. Epithelial-mesenchymal transition (EMT) is regarded as the beginning of invasion and metastasis and has been implicated in the metastasis of bladder cancer. We therefore postulate that RI regulates EMT of bladder cancer cells. We find that the over-expression of RI induces the up-regulation of E-cadherin, accompanied with the decreased expression of proteins associated with EMT, such as N-cadherin, Snail, Slug, vimentin and Twist and of matrix metalloprotein-2 (MMP-2), MMP-9 and Cyclin-D1, both in vitro and in vivo. The up-regulation of RI inhibits cell proliferation, migration and invasion, alters cell morphology and adhesion and leads to the rearrangement of the cytoskeleton in vitro. We also demonstrate that the up-regulation of RI can decrease the expression of integrin-linked kinase (ILK), a central component of signaling cascades controlling an array of biological processes. The over-expression of RI reduces the phosphorylation of the ILK downstream signaling targets p-Akt and p-GSK3β in T24 cells. We further find that bladder cancer with a high-metastasis capability shows higher vimentin, Snail, Slug and Twist and lower E-cadherin and RI expression in human clinical specimens. Finally, we provide evidence that the up-regulation of RI inhibits tumorigenesis and metastasis of bladder cancer in vivo. Thus, RI might play a novel role in the development of bladder cancer through regulating EMT and the ILK signaling pathway.
机译：人核糖核酸酶抑制剂（RI）是一种胞质酸性蛋白，可能与抑制RNase A和血管生成素活性不同，而具有生物学功能。先前我们已经证明RI可以抑制某些癌细胞的生长和转移。上皮-间质转化（EMT）被认为是侵袭和转移的开始，并且已经与膀胱癌的转移有关。因此，我们假设RI调节膀胱癌细胞的EMT。我们发现RI的过度表达诱导E-钙粘蛋白的上调，并伴随着与EMT相关的蛋白质（例如N-钙粘蛋白，Snail，Slug，波形蛋白和扭曲）和基质金属蛋白2（ MMP-2），MMP-9和Cyclin-D1，无论是在体内还是体外。 RI的上调抑制细胞增殖，迁移和侵袭，改变细胞形态和粘附并导致体外细胞骨架的重排。我们还证明，RI的上调可以降低整联蛋白连接激酶（ILK）的表达，整联蛋白连接激酶（ILK）是控制一系列生物过程的信号级联的重要组成部分。 RI的过度表达降低了T24细胞中ILK下游信号传导靶标p-Akt和p-GSK3β的磷酸化。我们进一步发现，具有高转移能力的膀胱癌在人类临床标本中显示出较高的波形蛋白，蜗牛，Slug和Twist以及较低的E-钙粘蛋白和RI表达。最后，我们提供的证据表明，RI的上调在体内抑制了膀胱癌的发生和转移。因此，RI可能通过调节EMT和ILK信号通路在膀胱癌的发展中发挥新作用。

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