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.
U87 cell low mesenchymal profile expressed high levels of kinin receptor 1 (B1R) and their invasion was greatly enhanced by the B1R agonist des-Arg<sup>9</sup>-bradykinin upon BM-MSC co-culturing in 3D co-cultures.
Accordingly, in the coculture EcTI also enhanced Ca<sup>2+</sup> signalling mediated <i>via</i> bradykinin receptor 2, being associated with nitric oxide release that highly impaired proliferation and invasion.
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.
We previously demonstrated that domain 5 (D5(H)), a functional domain of HK, and its derived peptides played an important role in the vitronectin-mediated suppression of cancer cell adhesion and invasion.
Invasion competence correlated with the parasites' ability to liberate the short-lived kinins from cell-bound kininogen and to elicit vigorous intracellular free calcium ([Ca(2+)](i)) transients through B(2)R. Invasion was impaired by membrane-permeable cysteine proteinase inhibitors such as Z-(SBz)Cys-Phe-CHN(2) but not by the hydrophilic inhibitor 1-trans-epoxysuccinyl-l-leucyl-amido-(4-guanidino) butane or cystatin C, suggesting that kinin release is confined to secluded spaces formed by juxtaposition of host cell and parasite plasma membranes.