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首页> 外文期刊>Cell biology international. >Polarization, migration, and homotypical interactions among prostatic smooth muscle cells in a laminin 111-rich extracellular matrix
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Polarization, migration, and homotypical interactions among prostatic smooth muscle cells in a laminin 111-rich extracellular matrix

机译：层压蛋白111-富含细胞外基质中前列腺平滑肌细胞之间的极化，迁移和均型相互作用

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摘要

Prostate cancer is a life-threatening condition worldwide. As the tumor progresses, smooth muscle cells (SMCs) become atrophic/dedifferentiated, within a series of stromal changes named stromal reaction. Here, we tested whether a laminin 111-rich extracellular matrix (Lr-ECM) could affect SMCs phenotype and differentiation status. Using time-lapse microscopy, image analyses, quantitative real-time reverse transcription polymerase chain reaction, immunohistochemistry and immunoblotting, and transmission electron microscopy, we showed that SMCs acquires a migratory behavior with a decreased expression of differentiation markers and relocation of focal adhesion kinase. SMCs set homotypic cell junctions and were active in autophagy/phagocytosis. Analysis of the migratory behavior showed that SMCs polarized and migrated toward each other, recognizing long-distance signals such as matrix tensioning. However, half of the cell population were immotile, irrespective of the nearest neighbor distance, suggesting they do not engage in productive interactions, possibly as a result of back-to-back positioning. In conclusion, the Lr-ECM, mimics the effects of the proliferating and infiltrating tumor epithelium, causing SMCs phenotypical change similar to that observed in the stromal reaction, in addition to a hitherto undescribed, stereotyped pattern of cell motility resulting from cell polarization.
机译：前列腺癌在世界范围内是一种威胁生命的疾病。随着肿瘤的进展，平滑肌细胞（SMC）在一系列称为基质反应的基质变化中萎缩/去分化。在这里，我们测试了富含层粘连蛋白111的细胞外基质（Lr-ECM）是否会影响SMC表型和分化状态。利用延时显微镜、图像分析、实时定量逆转录聚合酶链反应、免疫组织化学和免疫印迹以及透射电镜，我们发现SMC具有迁移行为，分化标记物表达减少，粘着斑激酶重新定位。平滑肌细胞建立了同型细胞连接，并在自噬/吞噬中表现活跃。对迁移行为的分析表明，SMC极化并向彼此迁移，识别出长距离信号，如基质张力。然而，有一半的细胞群是不动的，无论最近邻的距离如何，这表明它们不参与生产性的相互作用，这可能是背靠背定位的结果。总之，Lr ECM模拟增殖和浸润的肿瘤上皮细胞的作用，导致SMC表型变化，与基质反应中观察到的相似，此外，细胞极化导致了迄今为止尚未描述的细胞运动模式。

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