Knockdown of FOXM1 suppresses cell growth and metastasis in human laryngeal cancer via the AKT signaling pathway.

Abstract

This study aims to investigate the potential regulatory effect of forkhead box M1 (FOXM1) on laryngeal carcinoma (LC) and the underlying mechanisms. Tumor tissues were obtained from 80 patients diagnosed with LC in our hospital. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot analysis were used to detect the expression levels of FOXM1 in LC tissues and cell lines. Transfection of small interfering RNA (si-RNA) was conducted to knockdown the expression level of FOXM1. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay and cell colony assay were conducted to measure the changes in cell proliferation capacity influenced by FOXM1. Finally, invasion and migration ability was evaluated by the transwell assay. FOXM1 was found upregulated in LC tissues and cells. Transfection of FOXM1 siRNA in LC cells successfully inhibited the expression of FOXM1. The knockdown of FOXM1 resulted in reduced proliferation, invasion, and migration of LC cells. Further studies indicated that the knockdown of FOXM1 suppressed the ratio of p-AKT/AKT. Besides, the impaired proliferation, invasion, and migration of LC cells induced by FOXM1 knockdown could be counteracted by application of the AKT activator Sc79. The present work demonstrated that the knockdown of FOXM1 suppressed the proliferation, invasion, and migration of LC cells by the AKT signaling pathway.