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

Cancer cell | Jul 8, 2008

http://www.ncbi.nlm.nih.gov/pubmed/18598946

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.

Pubmed ID: 18598946 RIS Download

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

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