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AmotP130 regulates Rho GTP ase and decreases breast cancer cell mobility
Author(s) -
Chen ZheLing,
Yang Jiao,
Shen YanWei,
Li ShuTing,
Wang Xin,
Lv Meng,
Wang BiYuan,
Li Pan,
Zhao Wen,
Qiu RuiYue,
Liu Yu,
Liu PeiJun,
Yang Jin
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13533
Subject(s) - actin cytoskeleton , cytoskeleton , breast cancer , biology , cell migration , microbiology and biotechnology , motility , metastasis , actin , focal adhesion , cancer research , cancer cell , cancer , angiogenesis , cell , signal transduction , biochemistry , genetics
Angiomotin (Amot) is a newly discovered, multifunctional protein that is involved in cell migration and angiogenesis. However, the role of its isoform, AmotP130, in the regulation of cytoskeleton and metastasis of breast cancer, is unclear. The aim of this study was to investigate the role of AmotP130 in the reorganization of the actin cytoskeleton and the changes of morphology in breast cancer cells through the Rho pathway that influences the invasion and migration of cells. The results suggested that AmotP130 suppressed the invasion ability through remodelling the cytoskeleton of breast cancer cells, including the actin fibre organization and focal adhesion protein turnover. Global transcriptome changes in breast cancer cells following knockdown of AmotP130 identified pathways related with the cytoskeleton and cell motility that involved the Rho GTP ase family. From database analyses, changes in the Rho GTP ase family of proteins were identified as possible prognostic factors in patients with breast cancer. We have been suggested that AmotP130 suppressed the invasion ability through remodelling of the cytoskeleton of breast cancer cells, involving regulation of the Rho pathway. The cytoskeleton‐related pathway components may provide novel, clinically therapeutic targets for breast cancer treatment.

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