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TEEG Induced A549 Cell Autophagy by Regulating the PI3K/AKT/mTOR Signaling Pathway.
Analytical Cellular Pathology ( IF 3.2 ) Pub Date : 2019-04-30 , DOI: 10.1155/2019/7697610
Lu Shi 1 , Yijun Tu 2 , Yu Xia 2 , Siqi Ye 3 , Chaozhi Ma 2 , Yanwen Liu 2 , Pengtao You 2
Affiliation  

TEEG (3β,16β,23-trihydroxy-13,28-epoxyurs-11-ene-3-O-β-D-glucopyranoside) is derived from the chloroform extract of the Chinese medicine formula Shenqi San (CE-SS). In the present study, we aimed to elucidate the anticancer effect and possible molecular mechanism underlying the action of TEEG against the human non-small cell lung cancer (NSCLC) cell line A549 in vitro. A549 cells were incubated with different concentrations of TEEG. Cell proliferation was assessed by MTT assay. Autophagy was evaluated by immunofluorescence staining. Autophagy-associated proteins were examined by Western blot analysis. TEEG markedly inhibited A549 cell proliferation in a concentration-dependent manner. Immunofluorescence staining showed that TEEG induced autophagy in A549 cells. The LC3-II : LC3-I conversion ratio and the expression of Beclin-1, Atg5, Atg7, and Atg12 increased with the concentration of TEEG. In addition, increased TEEG concentration enhanced the expression of Class III p-PI3K and reduced the expression of Class I p-PI3K, p-AKT, p-mTOR, and p-P70S6K. These results indicate that TEEG induces autophagy of A549 cells through regulation of the PI3K/AKT/mTOR signaling pathway.

中文翻译:

TEEG通过调节PI3K / AKT / mTOR信号通路诱导A549细胞自噬。

TEEG(3 β,16 β,23三羟基13,28-epoxyurs -11-烯-3- O- β-D-吡喃葡萄糖苷)来源于中药配方肾气散(CE-SS)的氯仿提取物。在本研究中,我们旨在阐明TEEG在体外对人非小细胞肺癌(NSCLC)细胞系A549的抗癌作用和可能的分子机制。将A549细胞与不同浓度的TEEG一起孵育。通过MTT测定评估细胞增殖。通过免疫荧光染色评估自噬。通过蛋白质印迹分析检查自噬相关蛋白。TEEG以浓度依赖性方式显着抑制A549细胞增殖。免疫荧光染色显示TEEG诱导A549细胞自噬。LC3-II:LC3-I的转化率以及Beclin-1,Atg5,Atg7和Atg12的表达随TEEG浓度的增加而增加。此外,增加的TEEG浓度会增强III类p-PI3K的表达,并降低I类p-PI3K,p-AKT,p-mTOR和p-P70S6K的表达。这些结果表明TEEG通过调节PI3K / AKT / mTOR信号传导途径诱导A549细胞自噬。
更新日期:2019-04-30
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