| 庄建发,王艺辉,代玉娟,纪荣佳,陈大朝.索拉非尼与重组腺病毒H101对肝癌细胞株HepG2的作用及机制研究[J].,2018,(19):3742-3745 |
| 索拉非尼与重组腺病毒H101对肝癌细胞株HepG2的作用及机制研究 |
| Effect and Mechanism of Sorafenib and Recombinant Adenovirus H101 on Hepatocellular Carcinoma Cell Line HepG2 |
| 投稿时间：2018-03-02 修订日期：2018-03-26 |
| DOI：10.13241/j.cnki.pmb.2018.19.032 |
| 中文关键词: 肝癌细胞株HepG2 细胞凋亡 索拉非尼 重组腺病毒H101 作用机制 |
| 英文关键词: Hepatocellular carcinoma cell line HepG2 Apoptosis Sorafenib Recombinant adenovirus H101 Mechanism of action |
| 基金项目:漳州市2017年度自然科学基金项目（ZZ2017J39） |
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| 中文摘要: |
| 摘要 目的：研究索拉非尼与重组腺病毒H101对肝癌细胞株HepG2的作用并分析其具体机制。方法：选择索拉非尼、重组腺病毒H101分别组成重组腺病毒H101组、索拉非尼组、两药联合组以及空白对照组，并分别作用于购自中国科学院上海细胞生物研究所细胞库的肝癌细胞株HepG2。采用流式细胞技术检测HepG2细胞的凋亡情况；采用Western blot法检测细胞外信号调节激酶1/2（ERK1/2）、磷酸化ERK1/2（p-ERK1/2）以及髓样细胞白血病-1（Mcl-1）蛋白相对表达量；采用酶联免疫吸附法检测不同组别细胞培养上清液中的血管内皮生长因子（VEGF）水平。结果：重组腺病毒H101组、索拉非尼组、两药联合组的G0-G1期与G2-M期细胞均明显低于空白对照组，S期细胞均明显高于空白对照组，且两药联合组较重组腺病毒H101组与索拉非尼组更明显，差异均有统计学意义（均P<0.05）；重组腺病毒H101组、索拉非尼组、两药联合组的HepG2细胞凋亡率明显高于空白对照组，而两药联合组又明显高于重组腺病毒H101组与索拉非尼组，差异均有统计学意义（均P<0.05）。重组腺病毒H101组、索拉非尼组、两药联合组的p-ERK1/2、Mcl-1蛋白相对表达量和VEGF表达均明显低于空白对照组，而两药联合组又明显低于重组腺病毒H101组与索拉非尼组，差异均有统计学意义（均P<0.05）。结论：索拉非尼、重组腺病毒H101均可抑制肝癌细胞株HepG2的增殖，并诱导其凋亡，控制VEGF表达，联合应用具有更明显的效果，其主要机制可能与二者协同作用有效抑制p-ERK1/2、Mcl-1蛋白表达有关。 |
| 英文摘要: |
| ABSTRACT Objective: To study the effect of sorafenib and recombinant adenovirus H101 on hepatocellular carcinoma cell line HepG2 and to analyze its specific mechanism. Methods: Sorafenib, recombinant adenovirus H101 were used to form recombinant aden- ovirus H101 group, sorafenib group, two drug combination group and blank control group, and they were respectively acted on hepato- cellular carcinoma cell line HepG2 which were purchased from cell bank of Shanghai Institute of cell biology, Chinese Academy of Sci- ences. The apoptosis of HepG2 cells was detected by flow cytometry, the protein expression of extracellular signal regulated kinase 1/2 (ERK1/2), phosphorylated-ERK1/2 (p-ERK1/2), myeloid leukemia-1(Mcl-1) were detected using Western blot method, the levels of vas- cular endothelial growth factor (VEGF) in cell culture supernatant of different groups were detected by enzyme linked immunosorbent as- say. Results: The cells in G0-G1 and G2-M phase in the recombinant adenovirus H101 group, sorafenib group and two drug combination group were significantly lower than those in the blank control group, the cells in S phase were significantly higher than those in the blank control group, compared with the recombinant adenovirus H101 group and sorafenib group, the two drug combination group was more significantly, the differences were statistically significant (P<0.05). The apoptosis rate of HepG2 cells in recombinant adenovirus H101 group, sorafenib group and two drug combination group was significantly higher than that in the blank control group, the two drug com- bination group was significantly higher than the recombinant adenovirus H101 group and sorafenib group, the differences were statistically significant (P<0.05). The relative expression of p-ERK1/2 and Mcl-1 protein and the expression of VEGF in recombinant adenovirus H101 group, sorafenib group and two drug combination group were significantly lower than those in blank control group, the two drug combination group was significantly lower than the recombinant adenovirus H101 group and sorafenib group, the differences were statis- tically significant (P<0.05). Conclusion: Both sorafenib and recombinant adenovirus H101 can inhibit the proliferation of hepatoma cell line HepG2, induce apoptosis and control the expression of VEGF, the combined application has more obvious effect, and the main mechanism may be related to the synergistic effect of the two factors, which can effectively inhibit the expression of p-ERK1/2 and Mcl-1 proteins. |
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