MiR-338-3p improved lung adenocarcinoma by AKAP12 suppression.

ABSTRACT:

Introduction

This study aimed to explore the biological functions of AKAP12 in lung adenocarcinoma and investigate the interaction between AKAP12 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 AKAP12 expression in tumor tissues. The influences of AKAP12 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 AKA

SUBMITTER: Chang J 

PROVIDER: S-EPMC7959095 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature