Figure 6.
Effect of LCP1 I232F on cell migration and invasiveness. HeLa cells expressing wtLCP1 and LCP1 I232F were examined by using a scratch wound–healing assay at indicated time points (A), and results were analyzed graphically (n = 5) (B). Boyden chamber cell migration of HeLa (C) and 32D (D) cells (above) expressing wtLCP1 and LCP1 I232F. The assay was quantified by cell count and optical density (below). (E) Flow cytometry for the analysis of oxidative burst of indicated 32D cells, which were differentiated with 8 days of G-CSF treatment followed by stimulation with N-formyl-Met-Leu-Phe (fMLP) and phorbol myristate acetate (PMA). Oxidative burst was measured after treatment with dihydrorhodamine-123 (reported as mean fluorescence intensity [MFI] normalized to DFMO-treated samples). *P < .05, **P < .01, ***P < .001, ****P < .0001. DMSO, dimethyl sulfoxide; ns, not significant; PE, phycoerythrin; PE-A, Phycoerythrin-A.

Effect of LCP1 I232F on cell migration and invasiveness. HeLa cells expressing wtLCP1 and LCP1 I232F were examined by using a scratch wound–healing assay at indicated time points (A), and results were analyzed graphically (n = 5) (B). Boyden chamber cell migration of HeLa (C) and 32D (D) cells (above) expressing wtLCP1 and LCP1 I232F. The assay was quantified by cell count and optical density (below). (E) Flow cytometry for the analysis of oxidative burst of indicated 32D cells, which were differentiated with 8 days of G-CSF treatment followed by stimulation with N-formyl-Met-Leu-Phe (fMLP) and phorbol myristate acetate (PMA). Oxidative burst was measured after treatment with dihydrorhodamine-123 (reported as mean fluorescence intensity [MFI] normalized to DFMO-treated samples). *P < .05, **P < .01, ***P < .001, ****P < .0001. DMSO, dimethyl sulfoxide; ns, not significant; PE, phycoerythrin; PE-A, Phycoerythrin-A.

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