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首页> 外文期刊>Journal of biochemical and molecular toxicology >Autophagy induction and antiproliferative effect of a novel curcumin derivative MOMI‐1 on the human lung cancer cells A549
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Autophagy induction and antiproliferative effect of a novel curcumin derivative MOMI‐1 on the human lung cancer cells A549

机译：新型姜黄素衍生物MOMI-1对人肺癌细胞A549的自噬诱导和抗增殖效应

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Abstract To date, there are some chemically synthesized curcumin derivatives which were produced and identified to evade the disadvantages of physiochemical stability and solubility of curcumin. Here, one novel curcumin derivative, (2‐(3‐{(1E)‐{(E)‐3‐(4‐hydroxy‐3‐methoxybenzylidene)‐2‐oxocyclohexylidene)methyl)‐1H‐indol‐1‐yl)acetic acid}, (abbreviated as MOMI‐1) was first used to detect the antiproliferation activity with MTT assays in different cancer cells including A549 lung cancer cells, MCF‐7, and HEPG2 cell lines, and exhibited its wide inhibition spectrum. Next, we found that MOMI‐1 could induce autophagic genesis of A549 cells by acridine orange or monodansylcadaverine (MDC) staining and green fluorescent protein‐light chain 3 (GFP‐LC3) recombinant plasmid transfection analysis, respectively. Western blot analysis confirmed the LC3‐I/II conversion, beclin‐1 increase and p62 reduction of A549 cells after exposure of MOMI‐1, which suggested the typical autophagy induction. The following cell cycle test showed that MOMI‐1 could block A549 cells in G0/G1 phase. Furthermore, wounding healing experiment and transwell assays demonstrated that MOMI‐1 also possessed the antimigration ability of A549 cells. Our current results confirmed that MOMI‐1 could inhibit the proliferation and induce autophagy of A549 cells, which provide a new potential chemical candidate of antigrowth of A549 lung cancer cells. Future work needs to focus on the mechanism of autophagy pathway of A549 cells.
机译：迄今为止，存在一些化学合成的姜黄素衍生物，其产生并鉴定以避免生理化学稳定性和姜黄素溶解度的缺点。这里，一种新型姜黄素衍生物（2-（3 - {（1E） - {（e）-3-（4-羟基-3-甲氧基苄基）-2-氧和己基）甲基）-1H-吲哚-1-基）乙酸}（缩写为MOMI-1）首先用于检测不同癌细胞中的MTT测定的抗溶解活性，包括A549肺癌细胞，MCF-7和HepG2细胞系，并表现出其宽抑制谱。接下来，我们发现MOMI-1分别可以通过吖啶橙或单刚烷基碳酰胺（MDC）染色和绿色荧光蛋白 - 轻链3（GFP-LC3）重组质粒转染分析来诱导A549细胞的自噬生成。 Western印迹分析证实了LC3-I / II转化率，BECIN-1在MOMI-1暴露后的A549细胞增加和P62减少，这提出了典型的自噬诱导。以下细胞周期试验显示MOMI-1可以阻断G0 / G1相中的A549细胞。此外，伤口愈合实验和Transwell测定表明MOMI-1也具有A549细胞的抗疟功能。我们的目前的结果证实，MOMI-1可以抑制A549细胞的增殖和诱导自噬，这为A549肺癌细胞的抗重量进行了新的潜在化学候选者。未来的工作需要专注于A549细胞自噬途径的机制。

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