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      Induction of EMT by twist proteins as a collateral effect of tumor-promoting inactivation of premature senescence.

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          Abstract

          Twist1 and Twist2 are major regulators of embryogenesis. Twist1 has been shown to favor the metastatic dissemination of cancer cells through its ability to induce an epithelial-mesenchymal transition (EMT). Here, we show that a large fraction of human cancers overexpress Twist1 and/or Twist2. Both proteins override oncogene-induced premature senescence by abrogating key regulators of the p53- and Rb-dependent pathways. Twist1 and Twist2 cooperate with Ras to transform mouse embryonic fibroblasts. Interestingly, in epithelial cells, the oncogenic cooperation between Twist proteins and activated mitogenic oncoproteins, such as Ras or ErbB2, leads to complete EMT. These findings suggest an unanticipated direct link between early escape from failsafe programs and the acquisition of invasive features by cancer cells.

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          Author and article information

          Journal
          Cancer Cell
          Cancer cell
          Elsevier BV
          1878-3686
          1535-6108
          Jul 08 2008
          : 14
          : 1
          Affiliations
          [1 ] Inserm, U590, Lyon F-69008, France.
          Article
          S1535-6108(08)00195-5
          10.1016/j.ccr.2008.06.005
          18598946
          f4ebb678-8da9-4184-a681-9f3615e96aef
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