鉴定蛋白激酶C作为Na，K - ATP酶β亚基介导的板状伪足形成及癌细胞运动性抑制过程中的一种中间物质。
Identification of protein kinase C as an intermediate in Na,K-ATPase beta-subunit mediated lamellipodia formation and suppression of cell motility in carcinoma cells.
作者信息
Barwe S P, Rajasekaran S A, Rajasekaran A K
机构信息
Department of Pathology and Laboratory Medicine, University of California, Los Angeles, California 90095, USA.
出版信息
Cell Mol Biol (Noisy-le-grand). 2006 Dec 30;52(8):41-7.
We have shown that repletion of Na,K-ATPase Beta1-subunit (Na,K-Beta) in Moloney Sarcoma virus transformed MDCK (MSV-Na,K-Beta) cells induced lamellipodia and suppressed motility in a PI3-Kinase dependent manner. In this study, we provide evidence that decreased cell motility is due to increased attachment of Na,K-Beta expressing cells to the substratum. Treatment of MSV-Beta-GFP cells with bisindolylmalemide, a general Protein Kinase C (PKC) inhibitor, abolished PI3-Kinase activation and its down stream effects of Rac1 activation, binding of Na,K-Beta to annexin II, and suppression of cell motility and attachment. Thus, these studies unraveled that a PKC is involved upstream of PI3-Kinase in the suppression of Na,K-Beta mediated cell motility in carcinoma cells.
我们已经表明，在莫洛尼肉瘤病毒转化的MDCK（MSV-Na，K-Beta）细胞中补充Na，K-ATP酶β1亚基（Na，K-Beta）会以PI3激酶依赖性方式诱导片状伪足并抑制运动性。在本研究中，我们提供证据表明细胞运动性降低是由于表达Na，K-Beta的细胞与基质的附着增加所致。用双吲哚基马来酰胺（一种通用的蛋白激酶C（PKC）抑制剂）处理MSV-Beta-GFP细胞，消除了PI3激酶激活及其下游Rac1激活、Na，K-Beta与膜联蛋白II结合以及细胞运动性和附着抑制的影响。因此，这些研究揭示了PKC在PI3激酶上游参与抑制癌细胞中Na，K-Beta介导的细胞运动性。
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