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首页> 外文期刊>Journal of cellular physiology. >Metformin inhibition of colorectal cancer cell migration is associated with rebuilt adherens junctions and FAK downregulation
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Metformin inhibition of colorectal cancer cell migration is associated with rebuilt adherens junctions and FAK downregulation

机译：二甲双胍抑制大肠癌细胞迁移与重建adherens相关联连接和FAK downregulation

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E-cadherin, a central component of the adherens junction (AJ), is a single-pass trans-membrane protein that mediates cell-cell adhesion. The loss of E-cadherin surface expression, and therefore cell-cell adhesion, leads to increased cell migration and invasion. Treatment of colorectal cancer (CRC)-derived cells (SW-480 and HT-29) with 2.0 mM metformin promoted a redistribution of cytosolic E-cadherin to de novo formed puncta along the length of the contacting membranes of these cells. Metformin also promoted translocation from the cytosol to the plasma membrane of p120-catenin, another core component of the AJs. Furthermore, E-cadherin and p120-catenin colocalized with β-catenin at cell-cell contacts. Western blot analysis of lysates of CRC-derived cells revealed a substantial metformin-induced increase in the level of p120-catenin as well as E-cadherin phosphorylation on Ser~(838/840), a modification associated with β-catenin/ E-cadherin interaction. These modifications in E-cadherin, p120-catenin and β-catenin localization suggest that metformin induces rebuilding of AJs in CRC-derived cells. Those modifications were accompanied by the inhibition of focal adhesion kinase (FAK), as revealed by a significant decrease in the phosphorylation of FAK at Tyr~(397) and paxillin at Tyr~(118). These changes were associated with a reduction in the numbers, but an increase in the size, of focal adhesions and by the inhibition of cell migration. Overall, these observations indicate that metformin targets multiple pathways associated with CRC development and progression.
机译：钙adherens的核心组件结(AJ),是一个单程的转移膜蛋白介导信息附着力。钙粘蛋白表面的表情,因此信息粘连,导致增加细胞迁移和入侵。结直肠癌(CRC)派生细胞(sw - 480和HT-29)与2.0毫米二甲双胍促进了再分配新创的胞质钙粘蛋白形成puncta接触的长度这些细胞的细胞膜。从等离子体的胞质易位p120-catenin膜,另一个核心组件五角。p120-catenin与与β连环蛋白信息的联系人。CRC-derived细胞溶解产物显示大量的metformin-induced增加p120-catenin以及钙粘蛋白的水平磷酸化在Ser ~(838/840),修改与β连环蛋白/钙粘蛋白交互。p120-catenin和β连环蛋白定位建议二甲双胍诱发重建五角CRC-derived细胞。伴随着粘着斑的抑制激酶(FAK),揭示了一个重要的减少的FAK磷酸化酪氨酸~(397)和桩蛋白酪氨酸~(118)。变化与减少有关数字,但是增加大小,焦粘连细胞的抑制作用迁移。二甲双胍目标多个通路与CRC开发和进展有关。

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