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Archive > Volume 10 Issue 2 > 2018,10(2):214-221. DOI:10.1016/j.chmed.2018.03.007 Prev Next

Hederacolchiside A1通過調節(jié)PI3K / Akt / mTOR信號通路誘導腫瘤細胞凋亡

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Hederacolchiside A1 suppresses proliferation of tumor cells by inducing apoptosis through modulating PI3K/Akt/mTOR signaling pathway

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    摘要:
    目的：Hederacolchiside A1在體外對各種腫瘤細胞表現(xiàn)出細胞抑制和細胞毒活性，但其機制尚不清楚。本研究主要探討白頭翁中提取分離的Hederacolchiside A1的抗腫瘤活性和機制。 方法：用MTT法檢測Hederacolchiside A1對A549，SMMC-7721，BEL-7402和MCF-7細胞增殖的抑制作用。通過流式細胞術分析鑒定經(jīng)Hederacolchiside A1處理的腫瘤細胞凋亡狀況。 結果：根據(jù)Western blotting和JC-1染色結果：hederacolchiside A1降低腫瘤細胞線粒體膜電位和Bcl-2蛋白表達水平，并升高cleaved caspase-3蛋白表達水平。此外，hederacolchiside A1可有效地抑制磷脂酰肌醇（-3）激酶（PI3K），蛋白激酶B（Akt）和雷帕霉素靶蛋白（mTOR）表達水平。體內研究表明，在肝癌H22移植瘤模型中，Hederacolchiside A1（3.0，4.5和6.0mg / kg，ip）可顯著抑制腫瘤的重量；在人乳腺癌MCF-7移植瘤模型中，用Hederacolchiside A1（3.25,7.5和15.0mg / kg，ig）進行治療，觀察到類似的抑制活性。 結論：這些數(shù)據(jù)表明，Hederacolchiside A1可通過調節(jié)PI3K / Akt / mTOR信號傳導途徑誘導腫瘤細胞凋亡從而抑制腫瘤細胞的增殖。

    Abstract:
    Hederacolchiside A1, exhibits cytostatic and cytotoxic activity against various cancer cells in vitro, however, the mechanism is not well understood. In this study, Hederacolchiside A1 from Pulsatilla chinensis was isolated and tested its anticancer activity and mechanism. Hederacolchiside A1 could inhibit proliferation of A549, SMMC-7721, BEL-7402, and MCF-7 cells by MTT assay. Investigations of apoptosis of treated cancer cells were identified in hederacolchiside A1 by flow cytometric analysis of annexin V expression. Based on the results of western blotting and JC-1 staining, hederacolchiside A1 reduced the mitochondrial membrane potential and Bcl-2 protein levels, whereas cleaved caspase-3 was higher. Furthermore, hederacolchiside A1 effectively inhibited the phosphorylations of phosphatidylinositol 3 kinase (PI3K), protein kinase B (Akt), and mammalian target of rapamycin (mTOR). In vivo study showed that hederacolchiside A1 (3.0, 4.5, and 6.0 mg/kg, ip) could significantly inhibit the weight of tumor in an H22 xenograft model. Similar inhibitory activities were observed when the compound (3.25, 7.5, and 15.0 mg/kg, ig) was tested in nude mice xenograft tumor models using human breast carcinoma MCF-7 cells. These data indicated that hederacolchiside A1 suppressed the proliferation of human tumor cells by inducing apoptosis through modulating the PI3K/Akt/mTOR signaling pathway.

    關鍵詞:
    細胞凋亡; Hederacolchiside A1; 線粒體途徑;PI3K-Akt-mTOR途徑

    Keywords:


    Project Supported:
    This paper was funded by the National Sciences Foundation of China (No.81273402, 81573548).

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