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首页> 外文期刊>Cellular Physiology and Biochemistry >Metastasis Suppressor KAI1/CD82 Attenuates the Matrix Adhesion of Human Prostate Cancer Cells by Suppressing Fibronectin Expression and β 1 Integrin Activation
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Metastasis Suppressor KAI1/CD82 Attenuates the Matrix Adhesion of Human Prostate Cancer Cells by Suppressing Fibronectin Expression and β 1 Integrin Activation

机译：转移抑制因子KAI1 / CD82通过抑制纤连蛋白表达和β1整合素激活来减弱人前列腺癌细胞的基质粘附。

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KAI1/CD82, a tetraspanin membrane protein functions as a metastasis suppressor in many types of human cancers and has been shown to regulate cell adhesion properties. In the present study, we investigated the underlying mechanism of KAI1/CD82-mediated changes in cell adhesion to the extracellular matrix using human prostate cancer cells. We found that high KAI1/CD82 expression attenuated short-term cell adhesion to uncoated- or fibronectin-coated plates. Moreover, high KAI1/CD82 expression generated an extracellular environment unfavorable for cell adhesion as compared to low KAI1/CD82 expression, suggesting KAI1/CD82-dependent regulation of extracellular matrix (ECM) molecule(s) expression and/or secretion. Among ECM components examined, fibronectin exhibited decreased expression and secretion in high KAI1/CD82-expressing cells. Furthermore, high KAI1/CD82 expression interfered with the activation of β sub1/sub integrin at the cell surface while total β sub1/sub integrin levels remained unchanged, concomitant with reduced formation of focal adhesion complex and decreased bundling of actin filaments. Finally, high KAI1/CD82 expression significantly retarded cell motility in a scratch wound assay. Taken together, our results strongly suggest that KAI1/CD82 attenuates the activation of β sub1/sub integrin, and thereby down-regulates outside-in signaling of β sub1/sub integrin, leading to the reduction of focal adhesion formation and fibronectin expression/secretion, which subsequently interferes with cell adhesion properties and motility.
机译：KAI1 / CD82是一种四跨膜蛋白，在许多类型的人类癌症中均起转移抑制作用，并已证明可调节细胞粘附特性。在本研究中，我们调查了人类前列腺癌细胞对KAI1 / CD82介导的细胞粘附至细胞外基质的改变的潜在机制。我们发现高的KAI1 / CD82表达减弱了短期细胞对未包被或纤连蛋白包被的板的粘附。此外，与低KAI1 / CD82表达相比，高KAI1 / CD82表达产生不利于细胞粘附的细胞外环境，表明细胞外基质（ECM）分子表达和/或分泌的KAI1 / CD82依赖性调节。在所检查的ECM组件中，纤连蛋白在高表达KAI1 / CD82的细胞中表现出降低的表达和分泌。此外，高KAI1 / CD82表达会干扰细胞表面β 1 整合素的激活，而总β 1 整合素的水平却保持不变，并伴随着粘着斑形成的减少并减少肌动蛋白丝束。最后，在刮伤试验中，高KAI1 / CD82表达显着抑制了细胞运动。两者合计，我们的结果强烈表明，KAI1 / CD82减弱了β 1 整合素的激活，从而下调了β 1 整合素的外向内信号传导，导致了减少粘着斑形成和纤连蛋白的表达/分泌，继而干扰细胞的粘着性和运动性。

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