Yun-Bao Guo1, Xin-Jie Bao2, Song-Bai Xu1, Xing-Dong Zhang3, Hai-Yan Liu3. 1. Department of Neurosurgery, First Hospital of Jilin University Changchun 130021, China. 2. Department of Neurosurgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Peking Union Medical College Beijing 100730, China. 3. Department of Anatomy, College of Basic Medical Sciences, Jilin University Changchun 130021, China.
Abstract
OBJECTIVE: To investigate the signal pathway of honokiol-induced apoptosis in H4 human neuroglioma cells and to evaluate whether p53 signaling and cell cycle arrest were involved in honokiol-treated H4 human neuroglioma cells. METHODS: The cell viability was detected by the CCK8 assay. The cell apoptosis was assessed by annexin V-PI double-labeling staining and hoechst 33342 staining. The protein expression of cell cycle regulators and tumor suppressors were analyzed by western blotting. RESULTS: Treatment of H4 human neuroglioma cells with honokiol induced cell death in a dose-and time-dependent manner by using CCK8 assay. Consistent with the CCK8 assay, the flow cytometry results showed that the proportion of the apoptosis cells increased after honokiol when compared with untreated group. Moreover, H4 human neuroglioma cells exposed to honokiol, resulted in an accumulation of cells in S and G2/M phase. Apoptotic bodies were clearly observed in human neuroglioma cells when treated with honokiol and then stained with Hoechst 33342. The expression of Cyclin B1, CDC2 and cdc25C were downregulated, however, the expression of p-CDC2 and p-cdc25c was significantly upregulated when the neuroglioma cells were exposed to honokiol. Moreover, p53, p21 and Bax/Bcl-2 were significantly upregulated by honokiol treatment. CONCLUSIONS: These results confirmed that honokiol could induce apoptosis in human neuroglioma cells, the underlying molecular mechanisms, at least partially, through activation p53 signaling and induction of cell cycle arrest.
OBJECTIVE: To investigate the signal pathway of honokiol-induced apoptosis in H4 human neuroglioma cells and to evaluate whether p53 signaling and cell cycle arrest were involved in honokiol-treated H4 human neuroglioma cells. METHODS: The cell viability was detected by the CCK8 assay. The cell apoptosis was assessed by annexin V-PI double-labeling staining and hoechst 33342 staining. The protein expression of cell cycle regulators and tumor suppressors were analyzed by western blotting. RESULTS: Treatment of H4 human neuroglioma cells with honokiol induced cell death in a dose-and time-dependent manner by using CCK8 assay. Consistent with the CCK8 assay, the flow cytometry results showed that the proportion of the apoptosis cells increased after honokiol when compared with untreated group. Moreover, H4 human neuroglioma cells exposed to honokiol, resulted in an accumulation of cells in S and G2/M phase. Apoptotic bodies were clearly observed in human neuroglioma cells when treated with honokiol and then stained with Hoechst 33342. The expression of Cyclin B1, CDC2 and cdc25C were downregulated, however, the expression of p-CDC2 and p-cdc25c was significantly upregulated when the neuroglioma cells were exposed to honokiol. Moreover, p53, p21 and Bax/Bcl-2 were significantly upregulated by honokiol treatment. CONCLUSIONS: These results confirmed that honokiol could induce apoptosis in human neuroglioma cells, the underlying molecular mechanisms, at least partially, through activation p53 signaling and induction of cell cycle arrest.
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