Hsa-let-7c exerts an anti-tumor function by negatively regulating ANP32E in lung adenocarcinoma

We attempted to investigate the relationship between hsa-let-7c and ANP32E, as well as their influence on the cells phenotype of lung adenocarcinoma. Expression of hsa-let-7c and prognostic values were assessed by bioinformatics analysis based on TCGA database. Quantitative real-time PCR and western blot was employed to measure relative expression of hsa-let-7c or ANP32E. The targeting relationship between let-7c and ANP32E was predicted by biological software and validated by dual luciferase reporter assay. With gene transfection technology, cell proliferation, invasion and migration were appraised by cell counting Kit-8, clone formation and Transwell assays. The results showed that hsa-let-7c was downregulated in lung adenocarcinoma. Downregulation of hsa-let-7c notably led to a poor survival. ANP32E was forecasted and confirmed as a directly target of hsa-let-7c, and was upregulated in lung adenocarcinoma. Furthermore, upregulation of ANP32E had a significant correlation with unsatisfactory survival. Meanwhile, the levels of ANP32E were negatively regulated by hsa-let-7c. Upregulation of hsa-let-7c remarkably suppressed the Calu-3 cell proliferation, invasion and migration, while ANP32E overexpression plasmids rescued the downtrend. Inversely, hsa-let-7c silencing in NCI-H209 cells presented the opposite outcomes. Collectively, hsa-let-7c shows an anti-tumor effect in lung adenocarcinoma by targeting ANP32E and is expected to be a potential therapeutic target for lung adenocarcinoma.