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EGCG对鼻咽癌细胞增殖、凋亡及E2F-1表达的影响[J]. 肿瘤防治研究, 2012, 39(12): 1407-1410. DOI: 10.3971/j.issn.1000-8578.2012.12.001
引用本文: EGCG对鼻咽癌细胞增殖、凋亡及E2F-1表达的影响[J]. 肿瘤防治研究, 2012, 39(12): 1407-1410. DOI: 10.3971/j.issn.1000-8578.2012.12.001
Effect of EGCG on Proliferation,Apoptosis and E2F-1 Expression of Nasopharyngeal Carcinoma Cell[J]. Cancer Research on Prevention and Treatment, 2012, 39(12): 1407-1410. DOI: 10.3971/j.issn.1000-8578.2012.12.001
Citation: Effect of EGCG on Proliferation,Apoptosis and E2F-1 Expression of Nasopharyngeal Carcinoma Cell[J]. Cancer Research on Prevention and Treatment, 2012, 39(12): 1407-1410. DOI: 10.3971/j.issn.1000-8578.2012.12.001

EGCG对鼻咽癌细胞增殖、凋亡及E2F-1表达的影响

Effect of EGCG on Proliferation,Apoptosis and E2F-1 Expression of Nasopharyngeal Carcinoma Cell

  • 摘要: 目的 研究表没食子儿茶素没食子酸酯(EGCG)对鼻咽癌细胞增殖和凋亡的影响及其分子机制。方法采用CCK-8法检测EGCG对鼻咽癌细胞株CNE-2Z增殖的影响;AnnexinV /PI双标记流式细胞术检测EGCG的凋亡诱导作用;实时荧光定量PCR和Western blot检测核转录因子E2F-1及其上游调控蛋白CyclinD1和 p21的表达水平。结果EGCG处理后,CNE-2Z细胞的增殖明显受到抑制,其细胞凋亡率亦显著增高,呈量效关系;随着EGCG浓度增高,E2F-1 mRNA和蛋白表达水平明显下降,其上游调控蛋白CyclinD1的表达亦明显下调,而p21的表达则明显上调。结论EGCG可明显抑制鼻咽癌细胞增殖和诱导细胞凋亡,可能与其直接或间接下调核转录因子E2F-1有关,CyclinD1和p21参与其调控。

     

    Abstract: Objective To study the effects of epigallocatechin-3-gallate(EGCG)on proliferation and apoptosis of nasopharyngeal carcinoma cell and its mechanism. Methods The growth and proliferation of CNE-2Z cell was detected by CCK-8 assay,and apoptosis was assessed by AnnexinV/PI flow cytometry.The expressions of nuclear transcription factor E2F-1 and its regulatory protein CyclinD1 and p21 were detected by real-time quantitative PCR and Western blot. Results The proliferation of CNE-2Z cell was inhibited in a dose-dependent manner after treatment with EGCG,the apoptosis was induced as well.The expression of E2F-1 mRNA and protein in CNE-2Z cell were markedly suppressed by EGCG,and the level of its regulatory protein CyclinD1 also decreased while p21 was increased significantly. Conclusion EGCG suppressed the proliferation and induced apoptosis in CNE-2Z cell by directly or indirectly down-regulating E2F-1,which was regulated by CyclinD1 and p21.

     

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