张浩鹏,李国东,魏九峰.红树莓提取物抑制肝癌SMMC-7721细胞增殖的实验研究[J].中国肿瘤,2019,28(2):155-160. |
红树莓提取物抑制肝癌SMMC-7721细胞增殖的实验研究 |
Effect of Red Raspberry Extract on Proliferation of Human Hepatocellular Carcinoma SMMC-7721 Cells |
投稿时间:2018-05-09 |
DOI:10.11735/j.issn.1004-0242.2019.02.A015 |
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中文关键词: 红树莓提取物 肝肿瘤 细胞周期阻滞 |
英文关键词:red raspberry extract hepatocellular neoplasms cell cycle arrest |
基金项目:哈尔滨市科技创新人才研究专项资金项目(2017RAXXJ057);哈尔滨医科大学研究生创新科研项目(YJSCX2017-49HYD) |
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中文摘要: |
摘 要:[目的] 探讨红树莓提取物抑制肝癌SMMC-7721细胞增殖的具体机制,为红树莓提取物预防并治疗肝癌提供理论依据。[方法] 体外培养SMMC-7721细胞,应用CCK8方法及集落形成实验检测不同浓度的红树莓提取物对肝癌SMMC-7721细胞增殖活性的影响;通过流式细胞术检测SMMC-7721细胞经不同浓度的红树莓提取物作用72h后细胞周期的变化;应用Western blot方法检测红树莓提取物处理SMMC-7721细胞72h后细胞周期相关蛋白的表达变化,以及红树莓提取物对肝癌细胞AKT通路的影响。[结果] 红树莓提取物能够抑制SMMC-7721细胞的增殖活性;不同浓度红树莓提取物处理SMMC-7721细胞72h后,与对照组相比,随着浓度的增高,G0/G1期细胞数比例降低(P<0.05),S期细胞数比例升高(P<0.05);红树莓提取物能够降低周期相关蛋白cyclinA及CDK2的表达(P<0.01);同时使P-AKT(Ser473)表达下降(P<0.01)。[结论] 红树莓提取物能够抑制肝癌SMMC-7721细胞的增殖,这种抑制作用可能与AKT通路调控的cyclinA-CDK2介导的S期阻滞相关。 |
英文摘要: |
Abstract:[Purpose] To investigate the effect of red raspberry extract on the proliferation of human hepatocellular carcinoma SMMC-7721 cells. [Methods] Hepatocellular carcinoma SMMC-7721 cells were treated with different concentrations of red raspberry extract for 72h,the cell proliferation was detected by CCK8 and colony formation assay. The cell cycle of SMMC-7721 cells were detected by flow cytometry;the expression of proteins related to cell cycle and AKT pathway was detected by Western blot. [Results] Red raspberry extract inhibited the proliferation of SMMC-7721 cells. Compared with control group,the proportion of cells of G0/G1 phase in red raspberry extract-treatment groups was significantly decreased(P<0.05) and that of S phase increased(P<0.05). The expression of cyclinA and CDK2 as well as the expression of P-AKT (Ser473) in raspberry extract-treatment groups were decreased(P<0.01). [Conclusion] Red raspberry extract can inhibit the proliferation of human hepatocellular carcinoma SMMC-7721 cells,and the inhibitory effect is associated with S-phase arrest mediated by the AKT pathway. |
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