Loss of ASAP3 destabilizes cytoskeletal protein ACTG1 to suppress cancer cell migration
Loss of ASAP3 destabilizes cytoskeletal protein ACTG1 to suppress cancer cell migration
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DOI：
10.3892/mmr.2013.1831
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发表时间：
2014-02-01
影响因子：
3.4
通讯作者：
Yang, James Y.
中科院分区：
文献类型：
--
作者：
Luo, Yu;Kong, Fang;Yang, James Y.
具有SH 3结构域、锚蛋白重复序列和PH结构域3（ASAP 3）的ArfGAP，以前称为ACAP 4、DDEFL 1和UPLC 1，被认为是癌细胞迁移/侵袭和基于肌动蛋白的细胞骨架重塑的重要调节剂。然而，ASAP 3介导这些过程的潜在机制尚未得到很好的阐明。这项研究报告说，在某些类型的癌细胞中，ASAP 3的缺失抑制细胞迁移/侵袭，部分是通过使肌动蛋白-1（ACTG 1）不稳定，ACTG 1是一种细胞骨架蛋白，被认为是细胞迁移机制的组成部分，对动态细胞骨架网络的重排至关重要，在疾病中很重要，如脑畸形、听力损失和癌症发展。这些数据首次将ASAP 3与ACTG 1在细胞骨架维持和细胞运动调节中联系起来。
ArfGAP with SH3 domain, ankyrin repeat and PH domain 3 (ASAP3), previously known as ACAP4, DDEFL1 and UPLC1, is considered to be an important regulator in cancer cell migration/invasion and actin-based cytoskeletal remodeling. However, the underlying mechanisms through which ASAP3 mediates these processes are not well-elucidated. This study reported that in certain types of cancer cells, loss of ASAP3 suppressed cell migration/invasion, in part by destabilizing -actin-1 (ACTG1), a cytoskeletal protein considered to be an integral component of the cell migratory machinery, essential for the rearrangement of the dynamic cytoskeletal networks and important in diseases, such as brain malformation, hearing loss and cancer development. The data, for the first time, link ASAP3 with ACTG1 in the regulation of cytoskeletal maintenance and cell motility.