MiR-338-3p improved lung adenocarcinoma by suppression.

INTRODUCTION

This study aimed to explore the biological functions of in lung adenocarcinoma and investigate the interaction between and miR-338-3p.

MATERIAL AND METHODS

Sixty-one differentially expressed genes in lung adenocarcinoma and adjacent normal tissues were first analyzed by TCGA. Immunohistochemistry and quantitative reverse transcription PCR (qRT-PCR) were further utilized to confirm aberrant expression in tumor tissues. The influences of on proliferation, invasion and migration, and apoptosis of lung adenocarcinoma were investigated by clone formation assay and MTT assay, transwell assay, and flow cytometry analysis respectively. TargetScan and miRanda databases predicted the binding sites of miRNAs on 3'-UTR and structure changes were validated by RNA folding form. The target relationship between miR-338-3p and was confirmed by the dual-luciferase reporter system. Disease-free survival (DFS) and overall survival (OS) curves were generated with Kaplan-Meier plotter according to the TCGA data and the correlation among expression, miR-338-3p expression and prognosis was also analyzed.

RESULTS

was upregulated in lung adenocarcinoma tissues and cells (all < 0.01), and negatively correlated with prognosis outcomes of patients (both < 0.05). High expression of promoted proliferation, invasion and migration of cancer cells, and inhibited cell apoptosis (all < 0.05). MiR-338-3p could directly bind to the 3'-UTR of and showed most significant suppression on expression among four predicted miRNAs (all < 0.01). Additionally, miR-338-3p could suppress in lung adenocarcinoma, improving prognosis (all < 0.05).

CONCLUSIONS

acts as a tumor promoter in lung adenocarcinoma development. Upregulation of MiR-338-3p could suppress expression in lung cancer cells and contribute to a better prognosis.