Debmalya Roy 1,Qurat UI Ain 1,Ying-sheng Gao 1,Ghulam Jilany Khan 1,Sheng-tao Yuan2*,Li Sun 1*.Effect of Marsdenia tenacissima extract on G2/M cell cycle arrest by upregulating 14-3-3σ and downregulating c-myc in vitro and in vivo[J].Chinese Herbal Medicines (CHM),2019,11(2):169-176
Marsdenia tenacissima提取物在体内外水平通过上调14-3-3σ和下调c-myc影响细胞G2/M期周期阻滞
Effect of Marsdenia tenacissima extract on G2/M cell cycle arrest by upregulating 14-3-3σ and downregulating c-myc in vitro and in vivo
  
DOI:10.1016/j.chmed.2019.03.002
中文关键词:  G2/M期阻滞;MDA-MB-231;MCF7  Marsdenia tenacissima提取
英文关键词:c-myc  G2/M arrest  , , MCF-7  MDA-MB-231  Marsdenia tenacissima extract  14-3-3σ
基金项目:
Author NameAffiliation
Debmalya Roy 1 1Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China 
Qurat UI Ain 1 1Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China 
Ying-sheng Gao 1 1Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China 
Ghulam Jilany Khan 1 1Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China 
Sheng-tao Yuan2* 2Jiangsu Center for Pharmacodynamics Research and Evaluation, China Pharmaceutical University, Nanjing 210009, China. 
Li Sun 1* 1Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, Nanjing 210009, China 
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中文摘要:
      目的:MTE是有抗肿瘤活性的传统中草药提取物。先前的研究揭示了部分MTE抗肿瘤的机制。本研究首次发现MTE能够通过介导14-3-3σ和c-myc从而造成两种人乳腺癌细胞系MDA-MB-231和MCF7的G2/M期细胞周期阻滞。 方法:MTE对G2/M期细胞周期阻滞的影响在人乳腺癌细胞系MDA-MB-231和MCF7。MTT实验用于评价MTE对细胞活力的影响,流式细胞术用于评价MTE对细胞周期的影响。免疫蛋白印迹法和免疫组化用于探究细胞周期关键蛋白在细胞系和肿瘤组织中的表达情况。进行动物实验以探究MTE的抗肿瘤效应。 结果:细胞周期是肿瘤发展的基本过程。细胞周期蛋白在细胞周期和增殖中扮演关键角色。 有一些蛋白质直接或间接调节细胞周期关键蛋白。为了探究肿瘤细胞增殖,我们观察到MTE上调了14-3-3σ,下调了c-myc,并且抑制了G2/M期相关关键蛋白的表达,导致细胞阻滞在有丝分裂期。在MDA-MB-231的小鼠皮下移植瘤模型上,MTE表现出显著的抗肿瘤活性。 结论:MTE通过上调14-3-3σ和下调c-myc造成人乳腺癌细胞MDA-MB-231和MCF7的G2/M期阻滞。
英文摘要:
      Objective: Marsdenia tenacissima extract (MTE) is a traditional Chinese herbal medicine with anti-cancer activity. In some previous studies, different mechanism actions of the anti-cancer effect of MTE have been revealed. In this study, we first observed that MTE exhibits G2/M cell cycle arrest on two different human breast cancer cell lines, MDA-MB-231 and MCF-7 by mediating 14-3-3σ and c-myc. Methods: The effect of MTE on G2/M cell cycle arrest was evaluated in MDA-MB-231 and MCF-7 cell lines. MTT assay was done for evaluation of cell viability, Flow cytometry was employed for cell cycle analysis, Western blotting analysis and immunohistochemistry were performed to analyze the expression of G2/M cell cycle-related key protein in cells and tissue samples. Animal studies have been conducted to elucidate the anti-tumor effect of MTE. Results: Cell cycle is the backbone for developing cancer. Cell cycle proteins play a major role in the progression of cell cycle and cell proliferation. However, some key proteins directly or indirectly modulate the action of cell cycle protein that highly affect cell cycle regulation. In order to investigate cellular proliferation of cancer, we observed that MTE induced the upregulation of 14-3-3σ and downregulation of c-myc, and then reduced the expression of G2/M cell cycle associated key protein, leading to the inhibition of cellular entry into mitosis phase. We also confirmed that MTE exerted a significant antitumor effect on the MDA-MB-231 xenograft model in vivo. Conclusion: G2/M cell cycle arrest occurred by the action of MTE, mediated by the upregulation of 14-3-3σ as well as downregulation of c-myc in MDA-MB-231 and MCF-7 cell lines.
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