Paeoniflorin inhibits proliferation and promotes apoptosis of multiple myeloma cells via its effects on microRNA-29b and matrix metalloproteinase-2

Abstract

Multiple myeloma (MM) is a type of cancer characterized by the excessive proliferation of malignant plasma cells. In China, the incidence of MM has been increasing annually. Paeoniflorin exerts numerous functions, including coronary vessel expansion, and anti-inflammation andanticancer activities. The present study aimed to investigate the effects of paeoniflorin on the proliferation and apoptosis of SKO-007 MM cells, via its effects on the regulation of matrix metalloproteinase-2 (MMP-2) and microRNA (miR)-29b. In the present study, an MTT assay was used to analyze the proliferation of SKO-007 cells treated with paeoniflorin. Annexin V-fluorescein isothiocyanate/propidium iodide apoptosis and caspase-3 activation assays were used to detect the levels of cellular apoptosis. The expression levels of MMP-2 and miR-29b were detected using gelatin zymography and quantitative-polymerase chain reaction, respectively. In addition, miR-29b and anti-miR-29b plasmids were transfected into SKO-007 cells, and the effects of paeoniflorin on cell proliferation and apoptosis were subsequently detected. The results of the present in vitro studies demonstrated that paeoniflorin was able to inhibit the proliferation of SKO-007 cells in a dose-and time-dependent manner. Furthermore, paeoniflorin effectively increased cell apoptosis, and augmented the activation of caspase-3 and caspase-9 in the SKO-007 cells. The expression levels of MMP-2 were suppressed following treatment of the SKO-007 cells with paeoniflorin. In addition, paeoniflorin was able to induce the expression of miR-29b. Notably, the results of the present study indicated that miR-29b expression may control the expression of MMP-2 in SKO-007 cells. In conclusion, the present study demonstrated that paeoniflorin was able to inhibit cell proliferation and promote apoptosis of MM cells by suppressing the expression of MMP-2, via the upregulation of miR-29b.