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

Rac 和 PAK：连接解体和增加细胞运动性之间的合作伙伴关系

• 批准号: G0600791/1
• 负责人: Vania Braga
• 金额: $ 37.81万
• 依托单位: Imperial College London
• 依托单位国家: 英国
• 项目类别: Research Grant
• 财政年份: 2007
• 资助国家: 英国
• 起止时间: 2007 至 无数据
• 项目状态: 已结题
• 来源: https://gtr.ukri.org/projects?ref=G0600791%2F1
• 关键词: Rac; PAK; partnership; interface; between

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.

相邻细胞之间的紧密粘附在维持组织凝聚力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从实体瘤脱离和转移的关键事件。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侵袭的增加。类似的Rac过度活跃存在于许多不同类型的肿瘤中，并参与恶性转化。在这里，我们建议确定由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。