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Journal of Cellular Physiology

Journal of Cellular Physiology

IF: 4.5
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FMNL3 Promotes Migration and Invasion of Breast Cancer Cells via Inhibiting Rad23B‐Induced Ubiquitination of Twist1

Published:25 November 2024 DOI: 10.1002/jcp.31481 PMID: 39582466
Binggong Zhao, Dong‐Man Ye, Shujing Li, Yong Zhang, Yang Zheng, Jie Kang, Luhong Wang, Nannan Zhao, Bashir Ahmad, Jing Sun, Tao Yu, Huijian Wu

Abstract

Breast cancer is a heterogeneous malignant tumor, and its high metastasis rate depends on the abnormal activation of cell dynamics. Formin-like protein 3 (FMNL3) plays an important role in the formation of various cytoskeletons that participate in cell movement. The objective of this study was to explore the function of FMNL3 in breast cancer progression and endeavor to reveal the molecular mechanism of this phenomenon. We found that FMNL3 was abnormally highly expressed in aggressive breast cancer cells and tissues, and it significantly inhibited E-cadherin expression. FMNL3 could specifically interact with Twist1 rather than other epithelial-mesenchymal transition transcription factors (EMT-TFs). We also found that FMNL3 enhanced the repressive effect of Twist1 on CDH1 transcription in breast cancer cells. Further mechanism studies showed that FMNL3 suppressed the ubiquitin degradation of Twist1 by inhibiting the interaction between Twist1 and Rad23B, the ubiquitin transfer protein of Twist1. In vitro functional experiments, it was confirmed that FMNL3 promoted the migration and invasion of breast cancer cells by regulating Twist1. Furthermore, Twist1 could directly bind to the fmnl3 promoter to facilitate FMNL3 transcription. To conclude, this study indicated that FMNL3 acted as a pro-metastasis factor in breast cancer by promoting Twist1 stability to suppress CDH1 transcription.

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Materials
Procduct Name CAS Molecular Formula Supplier Price
MG-132 133407-82-6 C26H41N3O5 426 suppliers $11.00-$3568.00
FETUIN 9014-81-7 NULL 92 suppliers $37.07-$4810.00

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