Curcumin inhibits cell proliferation and induces apoptosis of human non-small cell lung cancer cells through the upregulation of miR-192-5p and suppression of PI3K/Akt signaling pathway
Curcumin inhibits cell proliferation and induces apoptosis of human non-small cell lung cancer cells through the upregulation of miR-192-5p and suppression of PI3K/Akt signaling pathway
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DOI：
10.3892/or.2015.4258
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发表时间：
2015-11-01
期刊：
影响因子：
4.2
通讯作者：
Shang, Yan
中科院分区：
文献类型：
--
作者：
Jin, Hai;Qiao, Fan;Shang, Yan
姜黄素是从中药姜黄中提取的主要活性成分，具有抗非小细胞肺癌细胞（NSCLC）、降血压、抗炎、利胆、抗氧化作用，长期无明显毒性。本研究的目的是探讨姜黄素的抗癌作用是否通过上调 microRNA-192-5p (miR-192-5p) 和抑制 PI3K/Akt 信号通路来抑制细胞增殖并诱导人 NSCLC 细胞凋亡。在本研究中，姜黄素处理抑制细胞增殖，诱导细胞凋亡并增加A549细胞的caspase-3活性。结果还显示，NCL-H460细胞的miR-192-5p相对表达量相对低于A549细胞，A549细胞的相对表达量较高，其中BEAS-2E细胞的表达量最高。 miR-192-5p 模拟抑制 A549 细胞的细胞增殖并增加细胞凋亡。然而，抗 miR-192-5p 模拟 A549 细胞的细胞增殖增加并抑制细胞凋亡。姜黄素治疗有效增加相对 miR-192-5p 表达并抑制 PI3K/Akt 信号通路。 miR-192-5p 模拟物增强姜黄素对细胞活力和细胞凋亡的影响，并抑制 A549 细胞中的 PI3K/Akt 信号通路。抗 miR-192-5p 模拟物逆转了姜黄素对 A549 细胞和 PI3K/Akt 表达的影响。总的来说，我们的研究结果表明姜黄素通过上调 miR-192-5p 和抑制 PI3K/Akt 信号通路来抑制细胞增殖并诱导人非小细胞肺癌细胞凋亡。
Curcumin is the main active ingredient extracted from the traditional Chinese medicine, turmeric, which acts against non-small cell lung cancer cell (NSCLC), lowers blood pressure, is anti-inflammatory, choleretic, and exerts anti-oxidant effects, without any obvious toxicity in the long term. The aim of the present study was to investigate whether the anticancer effect of curcumin inhibited cell proliferation and induced apoptosis of human NSCLC through the upregulation of microRNA-192-5p (miR-192-5p) and suppression of the PI3K/Akt signaling pathway. In the present study, treatment with curcumin inhibited cell proliferation, induced cell apoptosis and increased the caspase-3 activity of A549 cells. The results also showed that, miR-192-5p relative expression of NCL-H460 cells was relatively lower than that of A549 cells, which was higher, with that of BEAS-2E cells being the highest. miR-192-5p mimics suppressed cell proliferation and increased cell apoptosis of A549 cells. However, anti-miR-192-5p mimics increased cell proliferation and inhibited cell apoptosis of A549 cells. Curcumin treatment effectively increased the relative miR-192-5p expression and suppressed the PI3K/Akt signaling pathway. miR-192-5p mimics enhanced the effect of curcumin on cell viability and apoptosis and suppressed the PI3K/Akt signaling pathway in A549 cells. Anti-miR-192-5p mimics reversed the effect of curcumin on A549 cells and PI3K/Akt expression. Collectively, our findings suggested that curcumin inhibited cell proliferation and induced apoptosis of human non-small cell lung cancer cells through the upregulation of miR-192-5p and suppression of the PI3K/Akt signaling pathway.