Figure 8. Akt is responsible for PRDX1-related invasion and metastasis.

(A) F-actin Immunofluorescence staining was used to analyze the cell cytoskeleton reorganization. Overexpression or knockdown of Akt could rescue the phenotype induced by genetic manipulating PRDX1. In U2-OS^shPRDX1 cells, overexpression of Akt resulted the obvious reorganization of cytoskeleton and the cell morphology changed into more fibroblastic-like, while knockdown of Akt in SAOS-2^PRDX1 induces morphology regressed into cobbles-tone shape. (B and C) Wound healing and transwell assays showed that the overexpression of Akt in U2-OS^shPRDX1 could rescue the migration and invasion defects caused by knockdown of PRDX1 (left panel). Moreover, downregulation of Akt abolished the ability of migration and invasion in SAOS-2^PRDX1 cells (right panel).