ASAP1与FAK在肿瘤中的研究进展  

Research Progress of ASAP1 and FAK in Can-cer

作　　者：范静 王丰梅[1] 郑小影 徐梦蝶 冶俊玲[1] 

机构地区：[1]青海大学附属医院病理科,青海 西宁

出　　处：《临床医学进展》2023年第4期6450-6456,共7页Advances in Clinical Medicine

摘　　要：肿瘤的发生机制复杂,而肿瘤的播散更是一个多方面参与的过程,其中细胞骨架的失调及细胞外基质的破坏、上皮间质转化(Epithelial-mesenchymal transition, EMT)扮演的角色至关重要。ASAP1 (Arf糖激化因子GTP酶活化蛋白)通过定位于细胞膜内外,调整细胞骨架,改变细胞极性,最终导致肿瘤转移。黏着斑激酶(Focal adhesion kinas, FAK)可以与ASAP1结合形成复合物,参与调节细胞外基质(Extracellular matrix, ECM)的成分,影响肿瘤细胞微环境及细胞骨架重组,从而促进肿瘤细胞的转移。本文简要回顾了两种蛋白在一些肿瘤中的表达及新进展,希望能在肿瘤诊断及治疗上提供参考。The pathogenesis of tumor is complex, and the spread of tumor is a multi-faceted process, in which cytoskeletal disorders, destruction of extracellular matrix and epithelial interstitial transformation play crucial roles. ASAP1 (Arf glycoactivator GTPase activating protein) induces tumor metastasis by localizing inside and outside the cell membrane, modulating the cytoskeleton and changing cell polarity. FAK (adhesion spot kinase) can combine with ASAP1 to form a complex, which is involved in the regulation of extracellular matrix (ECM) components, influence tumor cell microenvironment and cytoskeletal recombination, and thus promote tumor cell metastasis. In this paper, the expres-sion of these two proteins in some tumors and their new development are reviewed, hoping to pro-vide reference for tumor diagnosis and treatment.

关 键 词：ASAP1 FAK 文献综述 

分 类 号：R73[医药卫生—肿瘤]