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Archive > Volume 11 Issue 2 > 2019,11(2):169-176. DOI:10.1016/j.chmed.2019.03.002 Prev Next

Marsdenia tenacissima提取物在體內(nèi)外水平通過上調(diào)14-3-3σ和下調(diào)c-myc影響細(xì)胞G2/M期周期阻滯

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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

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    摘要:
    目的：MTE是有抗腫瘤活性的傳統(tǒng)中草藥提取物。先前的研究揭示了部分MTE抗腫瘤的機(jī)制。本研究首次發(fā)現(xiàn)MTE能夠通過介導(dǎo)14-3-3σ和c-myc從而造成兩種人乳腺癌細(xì)胞系MDA-MB-231和MCF7的G2/M期細(xì)胞周期阻滯。 方法：MTE對(duì)G2/M期細(xì)胞周期阻滯的影響在人乳腺癌細(xì)胞系MDA-MB-231和MCF7。MTT實(shí)驗(yàn)用于評(píng)價(jià)MTE對(duì)細(xì)胞活力的影響，流式細(xì)胞術(shù)用于評(píng)價(jià)MTE對(duì)細(xì)胞周期的影響。免疫蛋白印跡法和免疫組化用于探究細(xì)胞周期關(guān)鍵蛋白在細(xì)胞系和腫瘤組織中的表達(dá)情況。進(jìn)行動(dòng)物實(shí)驗(yàn)以探究MTE的抗腫瘤效應(yīng)。 結(jié)果：細(xì)胞周期是腫瘤發(fā)展的基本過程。細(xì)胞周期蛋白在細(xì)胞周期和增殖中扮演關(guān)鍵角色。 有一些蛋白質(zhì)直接或間接調(diào)節(jié)細(xì)胞周期關(guān)鍵蛋白。為了探究腫瘤細(xì)胞增殖，我們觀察到MTE上調(diào)了14-3-3σ，下調(diào)了c-myc，并且抑制了G2/M期相關(guān)關(guān)鍵蛋白的表達(dá)，導(dǎo)致細(xì)胞阻滯在有絲分裂期。在MDA-MB-231的小鼠皮下移植瘤模型上，MTE表現(xiàn)出顯著的抗腫瘤活性。 結(jié)論：MTE通過上調(diào)14-3-3σ和下調(diào)c-myc造成人乳腺癌細(xì)胞MDA-MB-231和MCF7的G2/M期阻滯。

    Abstract:
    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.

    關(guān)鍵詞:
    G2/M期阻滯;MDA-MB-231;MCF7; Marsdenia tenacissima提取

    Keywords:


    Project Supported:
    Nanjing Sanhome Pharmaceutical Co., Ltd.

    Clc Number:

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