MiR-30 suppresses lung cancer cell 95D epithelial mesenchymal transition and invasion through targeted regulating Snail.

As an important factor regulating the epithelial mesenchymal transition (EMT) Snail is associated with lung cancer. Bioinformatics analysis showed that microRNA-30a (miR-30a) may target the 3'-UTR of Snail mRNA. It was exhibited that miR-30a down-regulation was related to tumor size, TNM stage, and poor prognosis of non-small cell lung cancer (NSCLC) patients, which suggests that miR-30a might participate in NSCLC attack. This study aims to explore the role of miR-30a and Snail in NSCLC invasion and metastasis.

NSCLC tumor and para-carcinoma tissues were collected from 46 patients to evaluate the miR-30a and Snail expressions. The targeted relationship between miR-30a and Snail was verified by using dual-luciferase reporter assay. 95D cells were cultured in vitro and transfected with miR-30a mimic or small interfere RNA targeting Snail (si-Snail). The expression of miR-30a, Snail, EMT-related factors, malignant growth, invasion, and apoptosis, were compared.

Snail was significantly up-regulated, while miR-30a was significantly reduced in NSCLC tissue. MiR-30a suppressed Snail expression by targeting the 3'-URT of Snail mRNA. 95D cells exhibited significantly higher Snail, N-cadherin, and vimentin levels, while lower miR-30a, E-cadherin, and occludin expressions were compared with 95C cells. 95D cells presented stronger malignant growth and invasive ability, whereas lower background apoptosis than 95C. MiR-30a mimic and/or si-Snail transfection significantly enhanced E-cadherin and occludin expression, while significantly declined N-cadherin and vimentin levels, thus weakening malignant growth and invasion and increasing cell apoptosis.

Snail up-regulated, while miR-30a declined in NSCLC tissue. MiR-30a may suppress Snail expression, restrain EMT, and inhibit lung cancer cell invasion.