# KIF23 Overexpression Promotes Cell Viability, Migration, and Invasion via the Wnt/β‐Catenin Signaling Pathway in Anaplastic Thyroid Carcinoma

## TL;DR

This study shows that KIF23 promotes aggressive thyroid cancer growth by activating specific cell signaling pathways and reducing oxidative stress.

## Contribution

The novel finding is that KIF23 promotes anaplastic thyroid carcinoma progression via the Wnt/β-catenin pathway and ferroptosis regulation.

## Key findings

- KIF23 overexpression increases cell viability, migration, and invasion in anaplastic thyroid carcinoma cells.
- KIF23 activity is linked to Wnt/β-catenin signaling and reduced oxidative stress via ferroptosis regulation.
- Inhibiting the Wnt/β-catenin pathway partially reverses KIF23's pro-cancer effects.

## Abstract

Anaplastic thyroid carcinoma (ATC) is a rare, aggressive cancer with a poor prognosis and limited treatment options. KIF23, a key regulator of cell division, has been implicated in tumor progression, but its role in ATC remains unclear. This study investigates the effects of KIF23 on ATC cell viability, migration, invasion, and signaling pathways.

ATC cell models were generated by transfecting cells with KIF23 silencing or overexpression plasmids. KIF23 expression was measured by RT‐qPCR and Western blot. Cell viability, oxidative stress, migration, and invasion were assessed using CCK‐8, ELISA, scratch, and Transwell assays. Wnt/β‐catenin pathway activation was analyzed by Western blot, and ferroptosis was induced by erastin.

Silencing KIF23 significantly decreased cell viability, increased oxidative stress, and reduced cell migration and invasion. Overexpression of KIF23 enhanced cell viability, migration, and invasion, and these effects were partially reversed by the Wnt/β‐catenin pathway inhibitor NTZ. KIF23 overexpression led to a decrease in intracellular ROS levels and reduced oxidative stress markers. Erastin treatment, in contrast, increased ROS levels, reduced cell viability, and suppressed migration and invasion. In the OE‐KIF23 + erastin group, erastin partially reversed the pro‐survival and pro‐motility effects of KIF23 overexpression, with ROS levels and functional readouts shifting toward those of erastin‐treated cells, indicating that KIF23 interacts with ferroptosis‐related oxidative stress regulation in ATC cells.

KIF23 regulates ATC cell viability, migration, and invasion via the Wnt/β‐catenin signaling pathway and ferroptosis. These findings suggest that KIF23 may be a potential therapeutic target for ATC treatment.