MiR-22 inhibits lung cancer cell EMT and invasion through targeting Snail.

OBJECTIVE: 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. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.