Abstract:Abstract: To investigate the role of ERK1/2 signaling pathway in TAM-induced apoptosis of glioma cells, MTT assay was performed to measure the viability of C6 and U87MG glioma cells treated with TAM. DAPI staining via inverted microscope and flow cytometry were used to detect the morphological changes of apoptosis and apoptotic rates, respectively. The phosphorylation of ERK1/2 was examined by Western-blot. Finally, flow cytometry was performed to evaluate the apoptosis of C6 and U87MG glioma cells co-treated with TAM and PD98059 (inhibitor of ERK1/2). The results showed that TAM dose- and time-dependently inhibited the glioma cell growth. The apoptosis of glioma cells treated with TAM was dose-dependently increased. Furthermore, ERK1/2 phosphorylation in cells treated with TAM was significantly higher than those in the controls. Additionally, blocking ERK1/2 activation with PD98059 obviously enhanced TAM-mediated apoptosis. These results indicated that TAM could inhibit the cell growth and induce apoptosis, and that activation of ERK1/2 signaling pathways could regulate TAM-induced glioma cell apoptosis.
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田 芬, 武慧姣, 谢富康, 李朝红. ERK1/2信号通路活化对Tamoxifen所致胶质瘤细胞凋亡的影响[J]. 生命科学研究, 2019, 23(5): 352-358.
TIAN Fen, WU Hui-jiao, XIE Fu-kang, LI Chao-hong. Effects of ERK1/2 Signaling Pathway Activation on TAM Induced Apoptosis of Glioma Cells. Life Science Research, 2019, 23(5): 352-358.