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      Bmi1 is essential in Twist1-induced epithelial-mesenchymal transition.

      Nature cell biology

      metabolism, Cadherins, genetics, Cell Line, Cell Transformation, Neoplastic, Chromatin Assembly and Disassembly, Down-Regulation, Epithelial Cells, pathology, Exons, Female, Genes, p16, Head and Neck Neoplasms, Humans, Male, Mesoderm, Middle Aged, Neoplasm Metastasis, Nuclear Proteins, Polycomb Repressive Complex 1, Prognosis, Promoter Regions, Genetic, Proto-Oncogene Proteins, Repressor Proteins, Transcription, Genetic, Twist Transcription Factor

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          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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          Journal
          10.1038/ncb2099
          20818389

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