Jilin Provincial Key Laboratory on Molecular and Chemical Genetic, The Second Hospital of Jilin University, Changchun, Jilin, China.
Eur Rev Med Pharmacol Sci. 2017 Aug;21(16):3598-3604.
Snail is an important factor in regulating epithelial mesenchymal transition (EMT). Its elevation is related to the enhancement of lung cancer invasion. MicroRNA-22 (MiR-22) plays a role in regulating lung cancer cell invasion. Bioinformatics analysis showed the complementary binding site between miR-22 and Snail. This study aimed to investigate the role of miR-22 in regulating Snail and affecting lung cancer cell invasion and metastasis.
Dual luciferase assay confirmed the targeted relationship between miR-22 and Snail. MiR-22 and Snail expressions were compared in MRC-5, Anip973, and AGZY83-a cells. Cell colony formation and invasion were tested in Anip973 and AGYZ83-a cells. Anip973 and AGYZ83-a cells were treated by 5 ng/ml transforming growth factor β1 (TGF-β1) to detect miR-22, Snail, E-cadherin, and N-cadherin expressions. Anip973 cells were cultured in vitro and divided into five groups, including miR-Normal control (miR-NC), miR-22 mimic, small interfering RNA-Normal control (si-NC), si-Snail, and miR-22 mimic + si-Snail groups.
MiR-22 targeted inhibited Snail expression. MiR-22 significantly down-regulated, while Snail obviously elevated in Anip973 and AGYZ83-a cells compared with that in MRC-5 cells. Anip973 exhibited markedly stronger invasive and colony formation abilities than AGYZ83-a. TGFβ1 apparently reduced miR-22 and E-cadherin, whereas increased Snail and N-cadherin stronger in Anip973 than that in AGYZ83-a. MiR-22 mimic and/or si-Snail transfection significantly reduced Snail and N-cadherin levels, up-regulated E-cadherin expression, and attenuated cell colony formation and invasion.
Down-regulation of miR-22 plays a role in facilitating lung cancer cell EMT and invasion by elevating Snail. MiR-22 over-expression attenuated lung cancer cell EMT and invasion via targeted inhibiting Snail.
蜗牛是调节上皮-间充质转化（EMT）的重要因素。其升高与肺癌侵袭增强有关。微小 RNA-22（MiR-22）在调节肺癌细胞侵袭中发挥作用。生物信息学分析显示 miR-22 与蜗牛之间存在互补结合位点。本研究旨在探讨 miR-22 在调节蜗牛并影响肺癌细胞侵袭和转移中的作用。
双荧光素酶测定证实了 miR-22 与蜗牛之间的靶向关系。比较 MRC-5、Anip973 和 AGZY83-a 细胞中的 miR-22 和 Snail 表达。在 Anip973 和 AGZY83-a 细胞中检测细胞集落形成和侵袭。用 5ng/ml 转化生长因子β1（TGF-β1）处理 Anip973 和 AGYZ83-a 细胞，检测 miR-22、Snail、E-钙粘蛋白和 N-钙粘蛋白的表达。在体外培养 Anip973 细胞，并将其分为 miR-正常对照（miR-NC）、miR-22 模拟物、小干扰 RNA-正常对照（si-NC）、si-Snail 和 miR-22 模拟物+si-Snail 组 5 组。
miR-22 靶向抑制 Snail 表达。与 MRC-5 细胞相比，miR-22 在 Anip973 和 AGYZ83-a 细胞中明显下调，而 Snail 明显上调。Anip973 比 AGYZ83-a 具有更强的侵袭和集落形成能力。TGFβ1 明显降低 miR-22 和 E-钙粘蛋白，而 Anip973 中 Snail 和 N-钙粘蛋白的增加明显强于 AGYZ83-a。miR-22 模拟物和/或 si-Snail 转染显著降低 Snail 和 N-钙粘蛋白水平，上调 E-钙粘蛋白表达，并减弱细胞集落形成和侵袭。
下调 miR-22 通过上调 Snail 促进肺癌细胞 EMT 和侵袭。miR-22 通过靶向抑制 Snail 过表达来减弱肺癌细胞 EMT 和侵袭。
