Abstract
Bradykinin (BK) has been reported to be involved in the progression of many types of cancer. In the present study, we investigated a possible role of BK in colorectal cancer cell invasion and migration. Invasion and migration assays showed that BK treatment promoted the invasion and migration of colorectal cancer cells. Further experiments showed that BK treatment stimulated ERK1/2 activation and IL-6 production. Two bradykinin receptors, bradykinin B1 receptor (B1R) and bradykinin B2 receptor (B2R), were significantly expressed in all the tested colorectal cancer cells. Repression of B2R, but not B1R, attenuated the BK-mediated invasion and migration, and inhibited ERK1/2 activation and IL-6 production. Moreover, blocking of the ERK pathway decreased the BK-mediated IL-6 production. In addition, IL-6 repression suppressed the effects of BK on colorectal cancer cell invasion and migration. Taken together, the present study demonstrated that BK increases IL-6 production via B2R and the ERK pathway, thereby contributing to the invasion and migration of colorectal cancer cells. Thus, our findings may provide benefits for the treatment of colorectal cancer.
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