KIF23 silencing suppresses papillary thyroid carcinoma metastasis by regulating mitophagy via Wnt/β-catenin pathway

作者：Ying Liu, Junping Zhang, Yuhang Chen, Mengya Zhu, Wen Chen, Zejin Hao, Yuanyuan Deng, Xiudan Han, Jixiong Xu · 发表于：Endocrine Connections · 年份：2025 · DOI：10.1530/ec-25-0090 · 被引用次数：2 · 研究领域：Microtubule and mitosis dynamics、Wnt/β-catenin signaling in development and cancer、Autophagy in Disease and Therapy

Background: Kinesin family member 23 (KIF23) plays a critical role in the regulation of cell division. This study aims to explore the function of KIF23 and its underlying regulatory mechanisms in the progression of papillary thyroid carcinoma (PTC). Methods: KIF23 expression was analyzed in PTC and adjacent tissues using RNA sequencing (RNA-Seq) data in The Cancer Genome Atlas (TCGA). Immunohistochemistry (IHC) and quantitative reverse transcription PCR (qRT-PCR) were performed to assess KIF23 expression in PTC tissues and cell lines. A KIF23 knockdown cell line was established to evaluate its effects on cell proliferation and migration via cell counting kit-8 (CCK-8), colony formation, Transwell migration, and wound-healing assays. Western blotting (WB) was used to analyze Wnt/β-catenin signaling and mitophagy markers. Results: KIF23 transcript levels were significantly elevated in PTC tissues compared to adjacent normal tissues, correlating with poor progression-free interval. IHC staining confirmed the upregulation of KIF23 in PTC tissues, while qRT-PCR analysis verified the increased mRNA expression of KIF23 in cell lines. KIF23 knockdown reduced cell proliferation, migration, and invasion and decreased levels of Wnt/β-catenin signaling proteins β-catenin (CTNNB1) and c-Myc (MYC) while increasing mitophagy markers Parkin (PRKN), PTEN-induced kinase 1 (PINK1), and LC3B (MAP1LC3B). Wnt agonist treatment reversed these effects, and both the Wnt agonist and the mitophagy inhi...