Abstract
It has been reported recently that bradykinin (BK) is involved in the regulation of various processes in cancer cells. However, its role and underlying mechanism of action in cervical cancer (CC) are still unknown. In the present study, it was revealed that BK promoted proliferation, migration, and invasion of CC cells, whereas bradykinin B2 receptor antagonist HOE140 had the inverse effect. Furthermore, it was confirmed that overexpression of bradykinin B2 receptor (B2R) facilitated the proliferation, migration, and invasion of BK-treated CC cells, while knockdown of B2R had the opposite effect. Mechanistically, the present results revealed that the BK/B2R-induced biological function of CC cells occured by activating STAT3 signaling pathways, and that knockdown of B2R or B2R antagonist had the opposite effects. Moreover, it was demonstrated that BK/B2R facilitated CC cell migration and invasion by upregulating the expression of the STAT3-regulated products MMP2 and MMP9, while downregulating the expression of the pro-apoptotic protein cleaved caspase-9. Thus, the present findings revealed that BK promoted CC cell proliferation, migration, and invasion by binding to B2R via STAT3 signaling pathways.
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