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In a recent clinical observation, the growth of endothelial tumors, such as nasopharyngeal carcinoma, was repressed by the non-selective-adrenergic antagonist propranolol. In this study, we evaluated whether β-adrenoceptors (β-ARs), nuclear factor κB (NF-κB), vascular endothelial growth factor (VEGF), cyclooxygenase-2 (COX-2), matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) were involved in modulating cell apoptosis and cell cycle arrest by propranolol in human gastric adenocarcinoma cell lines (SGC-7901 and BGC-823) in vitro. Our results showed that the propranolol treatment inhibited cell proliferation in a concentration-dependent manner, suggesting the involvement of β-ARs in this cellular response. Propranolol-induced growth inhibition was associated with G0/G1 arrest and G2/M arrest depending upon the concentration. In addition, propranolol also induced apoptosis in both cell lines, as determined by Annexin V staining assay. Furthermore, propranolol decreased the level of NF-κB and then downregulated VEGF, Cox-2, MMP-2 and MMP-9 expression. Collectively, these results suggested that propranolol repressed gastric cancer cell growth through the inhibition of β-ARs and the downstream NF-κB-VEGF/MMP-2/9/COX-2 pathway.

oncology reports

The β-adrenoceptor antagonist, propranolol, induces human gastric cancer cell apoptosis and cell cycle arrest via inhibiting nuclear factor κB signaling