Rac and PAK: a partnership at the interface between junction disassembly and increased cell motility

邻近细胞之间的紧密粘附在维持组织内聚和结构中起着重要作用。在肿瘤发生过程中，细胞-细胞粘附的破坏是细胞脱离实体瘤和转移的关键事件。我们发现Rac（一种信号蛋白）活性的增加导致细胞-细胞接触的快速不稳定以及细胞迁移和入侵的增加。在许多不同类型的肿瘤中都发现了类似的Rac高活性，并参与了恶性转化。在这里，我们建议鉴定Rac招募的调节分子，以帮助扰乱细胞-细胞接触稳定性，并研究它们在肿瘤发生过程中作为治疗靶点的潜力。

Tight adhesion between neighbouring cells plays an important role in the maintenance of tissue cohesion and architecture. During tumorigenesis, disruption of cell-cell adhesion is a key event for cell detachment from solid tumours and metastasis. We found that increased activity of Rac, a signalling protein, leads to a rapid destabilization of cell-cell contacts and increased migration and invasion of cells. Similar Rac hyper-activity is found in many different types of tumours and participate in malignant transformation. Here we propose to identify regulatory molecules that are recruited by Rac to help perturb cell-cell contact stability and investigate their potential as therapeutic targets during tumorigenesis.