Basson Marc D
Surgical Service, John D. Dingell VA Medical Center and Department of Surgery, Wayne State University, Detroit, Michigan 48201-1932, USA.
Cancer Res. 2008 Jan 1;68(1):2-4. doi: 10.1158/0008-5472.CAN-07-2992.
Increasing evidence suggests that tumor cells can regulate their own adhesion via intracellular signals that modulate integrin binding affinity. Although the full pathway has not yet been elucidated, the effects of pressure seem likely to require cytoskeletal mechanosensing, Src, phosphatidylinositol 3-kinase, focal adhesion kinase, and Akt-1 activation. Ultimately, activated focal adhesion kinase accumulates at the membrane in association with beta(1)-integrin heterodimers and may modulate integrin binding affinity. This pathway may be a promising target for manipulation to inhibit metastatic cancer cell adhesion.
越来越多的证据表明，肿瘤细胞可通过调节整合素结合亲和力的细胞内信号来调控自身的黏附。尽管完整的信号通路尚未阐明，但压力的作用似乎可能需要细胞骨架机械传感、Src、磷脂酰肌醇3激酶、黏着斑激酶和Akt-1激活。最终，激活的黏着斑激酶与β(1)-整合素异二聚体结合在细胞膜上聚集，并可能调节整合素的结合亲和力。该信号通路可能是抑制转移性癌细胞黏附的一个有前景的操作靶点。
