Genistein inhibits the proliferation of human multiple myeloma cells through suppression of nuclear factor-κB and upregulation of microRNA-29b

染料木素 细胞凋亡 细胞生长 碘化丙啶 细胞周期 生物 膜联蛋白 分子生物学 癌症研究 转染 程序性细胞死亡 细胞培养 内分泌学 生物化学 遗传学
作者
Jie Xie,Jianchao Wang,Bo Zhu
出处
期刊:Molecular Medicine Reports [Spandidos Publishing]
卷期号:13 (2): 1627-1632 被引量:36
标识
DOI:10.3892/mmr.2015.4740
摘要

Multiple myeloma (MM) is a malignant tumor and is the most common primary tumor of the bone marrow in the USA. Genistein is predominantly found in Leguminosae and various lines of evidence have indicated that it suppresses cell growth, induces programmed cell death and inhibits angiogenesis. As a result of these capabilities, genistein presents as a promising cancer chemopreventive agent. However, the effect of genistein on MM remains to be elucidated. The present study investigated the effect of genistein on the proliferation and apoptosis of MM cells through the regulation of nuclear factor-κB (NF-κB) and microRNA-29b (miR-29b). In the present study, cell proliferation was examined using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. In addition, apoptosis was detected using an Annexin V-fluorescein isothiocyanate/propidium iodide apoptosis assay and caspase-3 activation assay. The expression of NF-κB and miR-29b was analyzed using western blotting and reverse transcription quantitative polymerase chain reaction, respectively. Finally, miR-29b and anti-miR-29b plasmids were transfected into U266 cells to determine the effect of genistein on MM. In the present study, the results demonstrated that genistein could significantly reduce cell proliferation, induce apoptosis and increase the activity of caspase-3 in U266 cells. Furthermore, it was found that genistein could suppress the protein level of NF-κB and promote the expression of miR-29b in U266 cells. The results also indicated that miR-29b could alter the expression of NF-κB in U266 cells. These findings suggest that genistein inhibits the proliferation of human MM cells by upregulating miR-29b resulting in suppression of NF-κB.
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