Bmi1 is essential in Twist1-induced epithelial-mesenchymal transition

Muh Hwa Yang*, Dennis Shin Shian Hsu, Hsei Wei Wang, Hsiao Jung Wang, Hsin Yi Lan, Wen Hao Yang, Chi Hung Huang, Shou Yen Kao, Cheng Hwai Tzeng, Shyh Kuan Tai, Shyue Yih Chang, Oscar Kuang Sheng Lee, Kou Juey Wu

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

564 Scopus citations


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.

Original languageEnglish
Pages (from-to)982-992
Number of pages11
JournalNature Cell Biology
Issue number10
StatePublished - 10 2010
Externally publishedYes


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