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Oleanolic acid suppresses the proliferation of lung carcinoma cells by miR-122/Cyclin G1/MEF2D axis

机译:OLEALIC酸通过MIR-122 / CYCLIN G1 / MEF2D轴抑制肺癌细胞的增殖

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摘要

Oleanolic acid (OA) is a natural compound from plants with anti-tumor activities. However, the mechanism of the inhibitory effect of OA on cell cycle progression has not been completely explored. We employed several lung carcinoma cell lines to investigate the cell cycle-related molecular pathway affected by OA. The data revealed that OA suppressed the proliferation of lung cancer cells in both dose- and time-dependent manners, along with an increase in miR-122 abundance. The suppression of miR-122 abolished the effect of OA on lung cancer cells. CCNG1 and MEF2D, two putative miR-122 targets, were found to be downregulated by OA treatment. Restoring their expression counteracted the effect of OA on lung carcinoma cells. OA was further shown to induce the expression of miR-122-regulating transcriptional factors in lung cancer cells. Collectively, OA induced cell cycle arrest in lung cancer cells through miR-122/Cyclin G1/MEF2D pathway. This finding may contribute to the understanding of the molecular mechanism of OA's anti-tumor activity.
机译:Oleanolic acid(OA)是来自抗肿瘤活性植物的天然化合物。然而,OA对细胞周期进展的抑制作用的机制尚未完全探索。我们使用几种肺癌细胞系来研究受OA影响的细胞周期相关的分子途径。数据显示,OA以剂量和时间依赖的方式抑制了肺癌细胞的增殖,随着miR-122丰度的增加。 miR-122的抑制废除了OA对肺癌细胞的影响。 CCNG1和MEF2D,两个推定的MIR-122靶标被发现通过OA治疗来下调。恢复他们的表达抵消了OA对肺癌细胞的影响。进一步显示OA诱导肺癌细胞中miR-122调节转录因子的表达。通过MiR-122 / Cyclin G1 / MeF2D途径统称,OA诱导肺癌细胞中的细胞周期停滞。该发现可能有助于了解OA抗肿瘤活性的分子机制。

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