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

      Cancer Cell

      ras Proteins, Animals, Up-Regulation, metabolism, genetics, Twist Transcription Factor, Tumor Suppressor Protein p53, Transplantation, Heterologous, Transfection, Retinoblastoma Protein, Repressor Proteins, RNA Interference, Nuclear Proteins, pathology, enzymology, Neoplasms, Neoplasm Invasiveness, Mice, Transgenic, Mice, Nude, Mice, Inbred DBA, Mice, Inbred C57BL, Mice, Mammary Glands, Human, Humans, Gene Expression Regulation, Neoplastic, Fibroblasts, Epithelial Cells, Enzyme Activation, Dogs, Cell Transformation, Neoplastic, Cell Transdifferentiation, Cell Line, Cell Aging

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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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          Journal
          10.1016/j.ccr.2008.06.005
          18598946

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