Huang Chang-Lun, Ghule Shubham Suresh, Chang Yu-Hsiang, Tsai Hsiao-Chi, Lien Ming-Yu, Guo Jeng-Hung, Liu Chun-Lin, Liu Po-I, Tang Chih-Hsin
Division of General Thoracic Surgery, Department of Surgery, Changhua Christian Hospital, Changhua, Changhua 500, Taiwan, R.O.C.
Graduate Institute of Biomedical Science, China Medical University, Taichung 404328, Taiwan, R.O.C.
Oncol Rep. 2025 Oct;54(4). doi: 10.3892/or.2025.8961. Epub 2025 Aug 1.
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.
食管癌是全球最常见的癌症类型之一，常出现远处转移。脂肪因子内脂素与癌症进展和转移有关。然而，内脂素调节食管癌细胞运动的机制尚不清楚。生物信息学分析表明，转移性食管癌患者的内脂素水平高于原发性食管癌患者。细胞运动分析显示，内脂素刺激可增强食管癌细胞的迁移和侵袭能力。在KYSE410细胞中，用或不用内脂素（30 ng/ml）处理后进行miRNA测序，结果显示miR-3613-5p可调控内脂素诱导的细胞运动。进一步的细胞迁移、侵袭、qPCR和蛋白质印迹分析表明，内脂素通过降低miR-3613-5p的表达，进而增加血管内皮锌指蛋白1/多功能蛋白聚糖的产生，从而促进食管癌细胞迁移。因此，内脂素/miR-3613-5p轴可能是抑制食管癌细胞迁移和侵袭的一个有前景的靶点。
