Faculty of Biomedical Engineering, Toin University of Yokohama, 1614 Kurogane-cho, Aoba-ku, Yokohama, 225-8503, Japan.
Division of Materials Science, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma, 630-0192, Japan.
Mol Biol Rep. 2021 Mar;48(3):2291-2297. doi: 10.1007/s11033-021-06255-7. Epub 2021 Mar 6.
Apigenin is a flavonoid with antioxidant and anticancer effects. It has been reported that apigenin inhibits proliferation, migration, and invasion and induces apoptosis in cultured lung cancer cells. However, there is little information on the involvement of microRNAs (miRNAs) in its effects. miRNA microarray analysis and polymerase-chain-reaction analysis of miRNAs revealed that treatment of human lung cancer A549 cells with apigenin up-regulated the level of miR-34a-5p. Furthermore, mRNA microarray analysis and the results of three microRNA target prediction tools showed that Snail Family Transcriptional Repressor 1 (SNAI1), which inhibits the induction of apoptosis, had its mRNA expression down-regulated in A549 cells treated with apigenin. Our findings suggest that apigenin might induce apoptosis by down-regulation of SNAI1 through up-regulation of miR-34a-5p in A549 cells.
芹菜素是一种具有抗氧化和抗癌作用的类黄酮。据报道，芹菜素能抑制培养的肺癌细胞的增殖、迁移和侵袭，并诱导其凋亡。然而，关于其作用涉及 microRNAs（miRNAs）的信息很少。miRNA 微阵列分析和 miRNA 的聚合酶链反应分析显示，用芹菜素处理人肺癌 A549 细胞能上调 miR-34a-5p 的水平。此外，mRNA 微阵列分析和三种 microRNA 靶标预测工具的结果表明，抑制细胞凋亡诱导的 SNAI1（Snail Family Transcriptional Repressor 1）在芹菜素处理的 A549 细胞中的 mRNA 表达下调。我们的研究结果表明，芹菜素可能通过上调 miR-34a-5p 下调 SNAI1 诱导 A549 细胞凋亡。
