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Fig. 3 | BMC Cell Biology

Fig. 3

From: Prolactin-induced PAK1 tyrosyl phosphorylation promotes FAK dephosphorylation, breast cancer cell motility, invasion and metastasis

Fig. 3

Protein tyrosine phosphatase inhibition rescues PRL-mediated FAK auto-phosphorylation in T47D WT cells. a Tyrosine phosphatase inhibition by Na3VO4 permits PRL-induced FAK auto-phosphorylation in PAK1 WT cells. WCL of T47D PAK1 WT cells treated with either vehicle (veh) or Na3VO4 (100 ng/ml) for 1 h before PRL (200 ng/ml) treatment were probed for FAK auto-phosphorylation by αpY397-FAK antibody. b FAK is auto-phosphorylation in T47D GFP, PAK1 WT, and PAK1 Y3F cells in response to PRL in the presence of Na3VO4. The cells were treated with Na3VO4 as in A and with PRL (200 ng/ml) for the indicated times. FAK auto-phosphorylation was assessed as in A. The expression levels of γtubulin were used as an internal loading control. c Graph represents the densitometric analysis of the bands obtained for pY397-FAK normalized to total FAK for at least 3 independent experiments. Bars represent mean ± SE. *P < 0.05 compared with the same cells not treated with PRL

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