Visfatin facilitates esophageal cancer migration by suppressing miR‑3613‑5p expression and promoting VEZF1/VCAN production.

Abstract

Esophageal cancer, one of the most prevalent types of cancer worldwide, frequently exhibits distant metastases. The adipokine visfatin is implicated in cancer progression and metastasis. However, the mechanisms by which visfatin regulates motility in esophageal cancer remain unclear. Bioinformatics analysis showed levels of visfatin were higher in patients with metastatic esophageal cancer than in those with primary esophageal cancer. Cell motility assay revealed that visfatin stimulation enhanced the migration and invasion of esophageal cancer cells. Treatment with or without visfatin (30 ng/ml) in KYSE410 cells followed by miRNA sequencing, revealed that miR‑3613‑5p controlled visfatin‑induced cell motility. Further cell migration, invasion, qPCR and western blot assay shows that visfatin promoted esophageal cancer cell migration by decreasing miR‑3613‑5p expression and subsequently increasing vascular endothelial zinc finger 1/versican production. Thus, the visfatin/miR‑3613‑5p axis may be a promising target for inhibiting esophageal cancer cell migration and invasion.