Hsa‑miR‑216a‑3p regulates cell proliferation in oral cancer via the Wnt3a/β‑catenin pathway.

Abstract

Oral cancer is one of the leading causes of death worldwide, with a reported 5‑year survival rate of ~50% after treatment. The treatment measures for oral cancer are very expensive and affordability is low. Thus, it is necessary to develop more effective therapies to treat oral cancer. A number of studies have found that miRNAs are invasive biomarkers and have therapeutic potential in a variety of cancers. The present study included 30 oral patients and 30 healthy controls. Clinicopathological characteristic and miR‑216a‑3p/β‑catenin expression level of 30 oral cancer patients were analyzed. In addition, two oral cancer cell lines (HSC‑6 and CAL‑27) were used for mechanism‑of‑action study. The expression level of miR‑216a‑3p was higher in oral cancer patients compared with healthy controls and positively associated with tumor stage. Inhibition of miR‑216a‑3p potently suppressed cell viability and induced apoptosis of oral cancer cells. It was found that effects of miR‑216a‑3p on oral cancer were through Wnt3a signaling. It was also found that the expression level of β‑catenin was higher in oral cancer patients compared with healthy controls and positively associated with tumor stage; the effects of miR‑216a‑3p on oral cancer were through β‑catenin. In conclusion, miR‑216a‑3p and the Wnt‑β‑catenin signaling pathway may be interesting candidates to develop effective therapies for oral cancers.