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

doi:10.1038/ncb2099

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 journal › Article › peer-review

578 Scopus citations

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.

Original language	English
Pages (from-to)	982-992
Number of pages	11
Journal	Nature Cell Biology
Volume	12
Issue number	10
DOIs	https://doi.org/10.1038/ncb2099
State	Published - Oct 2010

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title = "Bmi1 is essential in Twist1-induced epithelial-mesenchymal transition",

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.",

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

year = "2010",

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doi = "10.1038/ncb2099",

language = "English",

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AU - Yang, Muh Hwa

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AU - Wang, Hsiao Jung

AU - Lan, Hsin Yi

AU - Yang, Wen Hao

AU - Huang, Chi Hung

AU - Kao, Shou Yen

AU - Tzeng, Cheng Hwai

AU - Tai, Shyh Kuan

AU - Chang, Shyue Yih

AU - Lee, Oscar Kuang Sheng

AU - Wu, Kou Juey

PY - 2010/10

Y1 - 2010/10

N2 - 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.

AB - 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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JO - Nature Cell Biology

JF - Nature Cell Biology

IS - 10

ER -

Bmi1 is essential in Twist1-induced epithelial-mesenchymal transition

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