Open AccessLoss of ASAP3 destabilizes cytoskeletal protein ACTG1 to suppress cancer cell migration
Author(s) -
Yu Luo,
Fang Kong,
Zhen Wang,
Dahan Chen,
Qiuyan Liu,
Tao Wang,
Rong Xu,
Xianyuan Wang,
James Y. Yang
Publication year - 2013
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2013.1831
Subject(s) - cytoskeleton , microbiology and biotechnology , biology , ankyrin repeat , cell migration , motility , cancer cell , actin , cell cycle , cell , cancer , cancer research , genetics , gene
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 γ-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.