# Low BOK Expression Promotes Epithelial–Mesenchymal Transition and Migration via the Wnt Signaling Pathway in Breast Cancer Cells

## TL;DR

Low BOK levels in breast cancer cells increase cell migration and EMT by activating the Wnt signaling pathway.

## Contribution

This study reveals a novel mechanism by which BOK regulates EMT and migration via the Wnt pathway in breast cancer.

## Key findings

- BOK overexpression inhibits EMT and migration in breast cancer cells.
- BOK silencing activates the Wnt signaling pathway and promotes EMT markers.
- Low BOK expression enhances breast cancer progression through Wnt pathway activation.

## Abstract

The B-cell lymphoma 2 (Bcl-2)-related ovarian killer (BOK), a member of the Bcl-2 protein family, shares a similar domain structure and amino acid sequence homology with the pro-apoptotic family members BAX and BAK. Although BOK is involved in the development of various types of cancer, its mechanism of action in breast cancer remains unclear. This study found that BOK was involved in the process of MG132, inhibiting the migration and epithelial–mesenchymal transition (EMT) of breast cancer cells induced by transforming growth factor-β. Furthermore, interfering BOK reversed the inhibition of breast cancer cell migration and the EMT process by MG132. Additional studies revealed that BOK silencing promoted the expression of EMT-related markers in breast cancer cells, while BOK overexpression inhibited EMT and migration. Using RNA-seq sequencing and Western blotting, we confirmed that the Wnt signaling pathway is involved in BOK regulating the EMT process in breast cancer cells. Therefore, we conclude that low BOK expression promotes breast cancer EMT and migration by activating the Wnt signaling pathway. This study enhances our understanding of breast cancer pathogenesis and suggests that BOK may serve as a potential prognostic marker and therapeutic target for breast cancer.