MiR-29c inhibits the metastasis of oral squamous cell carcinoma and promotes its cell cycle arrest by targeting SERPINH1.

BACKGROUND

A large number of studies have shown that the imbalance of micro RNA (miRNA) and its target genes can promote the development of tumors. The purpose of this study was to investigate the biological role and molecular mechanism of serpin peptidase inhibitor clade H member 1 (SERPINH1) and its upstream regulator miR-29c in oral squamous cell carcinoma (OSCC).

METHODS

The expression levels of SERPINH1 and miR-29c were detected by quantitative reverse transcription polymerase chain reaction (RT-qPCR) and western blotting. The proliferation, apoptosis, metastasis, and cell cycle were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, would healing assay, transwell assay, flow cytometry, and dual luciferase reporter assay.

RESULTS

High expression of SERPINH1 was detected in patients with OSCC and it can be used as a prognostic biomarker for OSCC. Cell function experiments showed that silencing the expression of SERPINH1 inhibited the proliferation and migration of OSCC cells and caused cell cycle arrest at S phase. Bioinformatics analysis showed that there was a binding site between miR-29c and SERPINH1, indicating that miR-29c may regulate the expression of SERPINH1. In addition, miR-29c overexpression inhibited the proliferation and metastasis of OSCC cells, and the subsequent rescue experiment showed that SERPINH1 overexpression can reverse the inhibitory effect of miR-29c in OSCC cell proliferation, migration, apoptosis, and cell cycle arrest.

CONCLUSIONS

The miRNA, miR-29c can regulate the proliferation, migration, invasion, and cell cycle of OSCC cells by targeting SERPINH1.