微小 RNA-140 通过下调 Smad3 表达抑制非小细胞肺癌细胞的迁移和侵袭。
MicroRNA-140's inhibition on the cell migration and invasion of non-small cell lung cancer by down-regulating Smad3 expression.
机构信息
Department of Respiratory (II), Linyi People's Hospital, Linyi, P.R. China.
出版信息
Eur Rev Med Pharmacol Sci. 2019 Nov;23(21):9471-9479. doi: 10.26355/eurrev_201911_19441.
OBJECTIVE
To investigate the effect of miR-140 on migration and invasion of non-small cell lung cancer (NSCLC) A549 cell and its regulatory mechanism.
MATERIALS AND METHODS
The NSCLC cell lines A549, H1650, NCI-H838, and normal lung epithelial cells BEAS-2B were purchased, and the expression of miR-140 and Smad3 in cells was detected by RT-PCR. MiR-140-inhibitor, miR-140-mimincs, miR-NC, sh-Smad3, Si-Smad3, and NC were transfected into A549 cells. Quantitative Real Time-Polymerase Chain Reaction (QRT-PCR) was used to detect the expression of miR-140 and Smad3. Transwell and cell scratch assay were used to detect cell invasion and migration. Dual-Luciferase report assay was used to study the relationship between mir-140 and Smad3.
RESULTS
MiR-140 was lowly expressed and Smad3 was highly expressed in NSCLC cells. Cell researches showed that the overexpression of miR-140 can inhibit cell invasion and migration. The downregulation of Smad3 expression inhibits cell invasion and migration. Dual-Luciferase reporter assay showed that miR-140 is a Smad3 targeting site.
CONCLUSIONS
MiR-140 can inhibit the invasion and migration of NSCLC cells by regulating Smad3, and it is expected to become a potential clinical target.
目的
研究 miR-140 对非小细胞肺癌（NSCLC）A549 细胞迁移和侵袭的影响及其调控机制。
材料与方法
购买 NSCLC 细胞系 A549、H1650、NCI-H838 和正常肺上皮细胞 BEAS-2B，通过 RT-PCR 检测细胞中 miR-140 和 Smad3 的表达。转染 miR-140 抑制剂、miR-140 模拟物、miR-NC、sh-Smad3、Si-Smad3 和 NC 至 A549 细胞。实时定量聚合酶链反应（QRT-PCR）用于检测 miR-140 和 Smad3 的表达。Transwell 和细胞划痕实验用于检测细胞侵袭和迁移。双荧光素酶报告实验用于研究 mir-140 和 Smad3 之间的关系。
结果
miR-140 在 NSCLC 细胞中低表达，Smad3 高表达。细胞研究表明，miR-140 的过表达可以抑制细胞侵袭和迁移。Smad3 表达下调抑制细胞侵袭和迁移。双荧光素酶报告实验表明，miR-140 是 Smad3 的一个靶位点。
结论
miR-140 可以通过调节 Smad3 抑制 NSCLC 细胞的侵袭和迁移，有望成为一种潜在的临床治疗靶点。
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