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Updated: Jun 9, 2026

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition
Published on: October 9, 2014
Bmi1 is essential in Twist1-induced epithelial-mesenchymal transition
Muh-Hwa Yang1, Dennis Shin-Shian Hsu, Hsei-Wei Wang
1Institute of Clinical Medicine, National Yang-Ming University, Department of Medicine, Taipei Veterans General Hospital, Taipei 112, Taiwan. mhyang2@vghtpe.gov.tw
Abstract:
The epithelial-mesenchymal transition (EMT), one of the main mechanisms underlying development of cancer metastasis, induces stem-like properties in epithelial cells. Bmi1 is a polycomb-group protein that maintains self-renewal, and is frequently overexpressed in human cancers. Here, we show the direct regulation of BMI1 by the EMT regulator, Twist1. Furthermore, Twist1 and Bmi1 were mutually essential to promote EMT and tumour-initiating capability. Twist1 and Bmi1 act cooperatively to repress expression of both E-cadherin and p16INK4a. In patients with head and neck cancers, increased levels of both Twist1 and Bmi1 correlated with downregulation of E-cadherin and p16INK4a, and was associated with the worst prognosis. These results suggest that Twist1-induced EMT and tumour-initiating capability in cancer cells occurs through chromatin remodelling, which leads to unfavourable clinical outcomes.
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