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Interleukin-5 (IL-5) plays an important role in the growth and differentiationof human B cells and eosinophils. However, little is known about the effect ofIL-5 on cancer cells. In this study, we investigated the molecular mechanismsinvolved in the IL-5-induced migration of HT1376 bladder cancer cells. Our resultsindicated that IL-5 significantly enhanced migration and MMP-9 expression in HT1376cells. We also found that IL-5 induces transcriptional activation of the bindingof NF-κB and AP-1, which are two important nuclear transcription factors thatare linked to MMP-9 expression in HT1376 cells. In subsequent experiments, wefound activation of ERK1/2 in IL-5-treated HT1376 cells. To examine the involvementof the ERK1/2 signaling pathway on IL-5-induced cell responses, we pretreatedHT1376 cells with the ERK1/2 inhibitor U0126 followed by IL-5 treatment. The resultsshowed that U0126 treatment inhibited migration of IL-5-treated HT1376 cells.Moreover, IL-5-stimulated MMP-9 expression was suppressed by the addition of U0126.Inhibition of ERK1/2 function consistently rescued transcriptional activity ofNF-κB, without altering AP-1 activation, in IL-5-treated cells. Finally, inhibitionof the IL-5-specific receptor IL-5Rα by small interfering RNA (siRNA) suppressedmigration, ERK1/2 activation, MMP-9 expression and binding activation of NF-κBin IL-5-treated HT1376 cells. The results of the present study indicate that theIL-28A/IL-28AR1 dyad induces cell migration through ERK1/2-mediated expressionof MMP-9 by binding activation of NF-κB in bladder cancer cells. In conclusion,these novel findings indicate that binding of IL-5 to IL-5Rα plays a criticalrole in MMP-9 expression, which may be involved in the migration of bladder cancer.

IL-5-induced migration via ERK1/2-mediated MMP-9 expression by inducing activation of NF-κB in HT1376 cells