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首页> 外文期刊>Genes to cells : >Over-expression of PAR-3 suppresses contact-mediated inhibition of cell migration in MDCK cells.
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Over-expression of PAR-3 suppresses contact-mediated inhibition of cell migration in MDCK cells.

机译：PAR-3的过表达抑制了MDCK细胞中细胞迁移的接触介导抑制。

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BACKGROUND: PAR-3 is one of the PAR proteins, previously named ASIP, which are indispensable for the establishment of cell polarity in the embryo as well as differentiated epithelial cells. In mammalian epithelial cells, it forms a ternary complex with aPKC and PAR-6, and is localized to the tight junction that has been suggested as being important for creating cell polarity. RESULTS: To gain insights into the mode of PAR-3 function in mammalian epithelial cells, we examined the effect of PAR-3 over-expression in MDCK cells. Although exogenous PAR-3-expression does not affect the epithelial polarity of confluent cells, it drastically transforms the morphology of cells at low density into a fibroblastic form with developed membrane protrusions. Time-lapse observations have revealed that PAR-3 over-expressing cells show intense motility, even after they have assembled into loose colonies, suggesting that the contact-mediated inhibition of cell migration (CIM) is suppressed. The expressions of E-cadherin and vimentin do not change with PAR-3 over-expression, suggesting that exogenous PAR-3 only disturbs the endogenous equilibrium of cellular states between a fundamental fibroblastic structure and an epithelial one. The co-expression of a dominant negative mutant of Rac1 and the addition of nocodazole strongly antagonize the effect of PAR-3 over-expression, suggesting the involvement of Rac1 activation and microtubule polymerizations. CONCLUSIONS: : The data presented here suggest an intriguing link between the contact-mediated inhibition of cell migration and the regulation of cell polarity. The putative PAR-3 activities demonstrated here may function endogenously in the epithelial cell polarization process by being sequestered from the cytosol to the cell-cell junctional regions with aPKC and PAR-6 upon cell-cell adhesion.
机译：背景：PAR-3是一种以前称为ASIP的PAR蛋白，对于在胚胎以及分化的上皮细胞中建立细胞极性是必不可少的。在哺乳动物上皮细胞中，它与aPKC和PAR-6形成三元复合物，并位于紧密连接处，该紧密连接已被认为对于产生细胞极性很重要。结果：为了深入了解PAR-3在哺乳动物上皮细胞中的功能模式，我们检查了PAR-3在MDCK细胞中过表达的影响。尽管外源PAR-3-表达不影响融合细胞的上皮极性，但它会以低密度将细胞形态急剧转变为成纤维细胞形式，并带有发达的膜突出物。延时观察表明，即使PAR-3过表达的细胞已经组装成松散的菌落，它们仍表现出强烈的运动能力，这表明接触介导的细胞迁移抑制（CIM）被抑制了。 E-钙黏着蛋白和波形蛋白的表达不会随着PAR-3的过表达而改变，这表明外源性PAR-3仅干扰基本的成纤维细胞结构和上皮细胞之间的细胞状态的内源性平衡。 Rac1的显性负突变体的共表达和诺考达唑的添加强烈拮抗PAR-3过表达的作用，表明Rac1激活和微管聚合反应的参与。结论：：这里提供的数据表明接触介导的细胞迁移抑制与细胞极性调节之间的有趣联系。此处证明的推定的PAR-3活性可能在上皮细胞极化过程中内源性发挥作用，因为在细胞与细胞之间的粘附作用下，其被aPKC和PAR-6从胞浆中隔离到细胞与细胞的连接区域。

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