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

机译:齐墩果酸通过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:齐墩果酸(OA)是来自植物的天然化合物,具有抗肿瘤活性。但是,尚未完全探讨OA对细胞周期进程的抑制作用机理。我们采用了几种肺癌细胞系来研究受OA影响的细胞周期相关分子途径。数据显示,OA以剂量和时间依赖性方式抑制肺癌细胞的增殖,同时增加miR-122的丰度。对miR-122的抑制消除了OA对肺癌细胞的作用。发现两个假定的miR-122靶标CCNG1和MEF2D被OA治疗下调。恢复它们的表达抵消了OA对肺癌细胞的作用。进一步显示OA可诱导肺癌细胞中miR-122调控转录因子的表达。总体而言,OA通过miR-122 / Cyclin G1 / MEF2D途径诱导肺癌细胞周期阻滞。这一发现可能有助于对OA抗肿瘤活性的分子机制的理解。

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