首页> 美国卫生研究院文献>American Journal of Translational Research >Babaodan inhibits cell growth by inducing autophagy through the PI3K/AKT/mTOR pathway and enhances antitumor effects of cisplatin in NSCLC cells
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Babaodan inhibits cell growth by inducing autophagy through the PI3K/AKT/mTOR pathway and enhances antitumor effects of cisplatin in NSCLC cells

机译:八宝丹通过PI3K / AKT / mTOR途径诱导自噬抑制细胞生长并增强顺铂在NSCLC细胞中的抗肿瘤作用

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摘要

Babaodan capsule (BBD), a traditional Chinese (TCM) formula, has been widely used as an alternative remedy for multiple types of malignancies, clinically. However, the underlying mechanisms behind the efficacy of BBD remain poorly understood, particularly in regard to lung cancer. Herein, we demonstrate that BBD induced autophagic death in A549 and A549DDP cells without apoptosis. Treatment with autophagic inhibitor 3-MA, Baf-A1 and PI3K agonist, IGF-1, fully proved our conclusion, as well as uncovered the potential downregulated signaling pathway, PI3K/AKT/mTOR. The study additionally found that BBD could downregulate the expression of MDR1 and increase the chemosensitivity of cisplatin. Collectively, our results, both in vivo and in vitro, demonstrate that BBD leads to autophagic cell death through downregulating the PI3K/AKT/mTOR signaling pathway and improved the antitumor effects of cisplatin in non-small cell lung cancer (NSCLC).
机译:八宝丹胶囊(BBD)是一种繁体中文(TCM)公式,在临床上已被广泛用作多种类型恶性肿瘤的替代疗法。然而,对BBD功效背后的潜在机制仍知之甚少,特别是在肺癌方面。在本文中,我们证明了BBD诱导了A549和A549DDP细胞自噬死亡,而没有凋亡。自噬抑制剂3-MA,Baf-A1和PI3K激动剂IGF-1的治疗充分证明了我们的结论,并揭示了潜在的下调信号通路PI3K / AKT / mTOR。研究还发现,BBD可以下调MDR1的表达并增加顺铂的化学敏感性。总体而言,我们的体内和体外研究结果表明,BBD通过下调PI3K / AKT / mTOR信号通路导致自噬细胞死亡,并改善了顺铂在非小细胞肺癌(NSCLC)中的抗肿瘤作用。

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