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　GTPase　family.　From　database　analyses,　changes　in　the　Rho　GTPase　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.