Fig. 2.

SOCS7 regulates TGF-β1-induced keratinocyte motility through the PI3K/AKT and MEK/ERK pathways. A. HaCaT cells were transfected with Vector or SOCS7 plasmids, and scrambled siRNA (siR-ctrl) or SOCS7 siRNA (siR-SOCS7) for 24 h, then treated with TGF-β1 (10 ng/ml) for 24 h. Protein expression levels of phosphorylated ERK1/2 (p‑ERK1/2), total ERK, phosphorylated AKT (p‑AKT) and total AKT were analyzed by western blotting (A). B–D. HaCaT cells were transfected with SOCS7 siRNA (siR-SOCS7) for 24 h, followed by LY294002 (10 μM) or U0126 (10 μM) for 1 h, then finally TGF-β1 (10 ng/ml) treatment for 24 h. Protein expression levels of phosphorylated ERK1/2 (p‑ERK1/2), total ERK, phosphorylated AKT (p‑AKT) and total AKT were analyzed by western blotting (B). Wound healing was assessed using the scratch‐wound assay. Representative images (left) and quantification of data showing the percentage of wound closure (right) (C). Cell migration was assessed using the Transwell migration assay. Representative images showing crystal violet staining (left) and quantification of data showing the number of migrated cells/field (right) (D). Data are given as mean ± standard deviation (SD) of three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001