摘要
目的:探讨FAK功能在ErbB2诱导肿瘤形成和侵袭过程中的作用。方法:采用FAK-/-和FAK+/+细胞感染含ErbB2逆病毒颗粒,使ErbB2在FAK-/-和FAK+/+细胞中过量表达,通过比较FAK-/-ErbB2和FAK+/+-ErbB2在细胞生存、细胞侵袭、体内成瘤等项指标来观察FAK的功能。结果:感染后,ErbB2受体在FAK-/-和FAK+/+细胞中稳定表达和激活。ErbB2诱导的锚定依赖性细胞生存、细胞侵袭以及体内肿瘤形成等方面均有赖于FAK功能。结论:FAK在调节ErbB2诱导的细胞生存、肿瘤形成和侵袭等方面起着重要的作用,其机制可能涉及到ErbB-FAK-Src-MAPK分子信号转导途径。
AIM ： To explore whether or not ErbB2 - induced oncogenic transformation and invasion are mediated by FAK. METHODS： Parental FAK^-/- and FAK^＋/＋ cells were used and infected with retrovector particles expressing ErbB2 in order to acquire ErbB2 - overexpressed cells, i.e. , FAK^-/- - ErbB2 and FAK^＋/＋ - ErbB2. The role of FAK signaling was explored by analyzing the parameters such as cell survival, invasiveness and tumorigenicity shown by both FAK^-/- and FAK^＋/＋ cells in which ErbB2 was overexpressed. RESULTS： ErbB2 was overexpressed and functionally activated in both FAK^-/- and FAK^＋/＋ cells upon infection with retrovector particles. The ErbB2 -induced anchorage -dependent cell survival, cell invasiveness as well as tumorigenicity in vivo were dependent on FAK. CONCLUSION： FAK is essential for cell survival, tumorigenicity and invasiveness induced by ErbB2, and its possible mechanism involves in ErbB - FAK - Src - MAPK pathway.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2007年第12期2369-2373,共5页
Chinese Journal of Pathophysiology
