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Cell migration is an essential step for tumor metastasis. The small  GTP ase  R ac1 plays an important role in cell migration. Previously, we reported that epidermal growth factor ( EGF ) induced two waves of  R ac1 activation; namely, at 5 min and 12 h after stimulation. A second wave of  EGF ‐induced  R ac1 activation was required for  EGF ‐induced cell migration, however, the spatiotemporal regulation of the second wave of  EGF ‐induced  R ac1 activation remains largely unclear. In this study, we found that 5‐lipoxygenase (5‐ LOX ) is activated in the process of  EGF ‐induced cell migration, and that leukotriene  C  4  ( LTC  4 ) produced by 5‐ LOX  mediated the second wave of  R ac1 activation, as well as cell migration. Furthermore, these effects caused by  LTC  4  were found to be blocked in the presence of the antagonist of cysteinyl leukotriene receptor 1 ( C ys LT 1). This blockage indicates that  LTC  4 ‐mediated  C ys LT 1 signaling regulates the second  EGF ‐induced wave of  R ac1 activation. We also found that 5‐ LOX  inhibitors,  C ys LT 1 antagonists and the knockdown of  C ys LT 1 inhibited  EGF ‐induced  T  cell lymphoma invasion and metastasis‐inducing protein 1 ( T iam1) expression.  T iam1 expression is required for the second wave of  EGF ‐induced  R ac1 activation in  A 431 cells. Therefore, our results indicate that the 5‐ LOX / LTC  4 /Cys LT 1 signaling pathway regulates  EGF ‐induced cell migration by increasing  T iam1 expression, leading to a second wave of  R ac1 activation. Thus,  C ys LT 1 may serve as a new molecular target for antimetastatic therapy. In addition, the  C ys LT 1 antagonist, montelukast, which is used clinically for allergy treatment, might have great potential as a novel type of antimetastatic agent.

cancer science

5‐Lipoxygenase and cysteinyl leukotriene receptor 1 regulate epidermal growth factor‐induced cell migration through  T iam1 upregulation and  R ac1 activation