Abstract
The plasticity of cancer cells underlies their capacity to adapt to the selective pressures they encounter during tumour development. Aberrant reactivation of epithelial-mesenchymal transition (EMT), an essential embryonic process, can promote cancer cell plasticity and fuel both tumour initiation and metastatic spread. Here we discuss the roles of EMT-inducing transcription factors in creating a pro-tumorigenic setting characterized by an intrinsic ability to withstand oncogenic insults through the mitigation of p53-dependent oncosuppressive functions and the gain of stemness-related properties.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Cell Differentiation
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Cell Transformation, Neoplastic / genetics
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Cell Transformation, Neoplastic / metabolism*
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Cell Transformation, Neoplastic / pathology
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Epithelial-Mesenchymal Transition* / genetics
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Gene Expression Regulation, Neoplastic
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Humans
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Neoplasm Invasiveness
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Neoplasms / genetics
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Neoplasms / metabolism*
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Neoplasms / pathology
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Neoplastic Stem Cells / metabolism
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Neoplastic Stem Cells / pathology
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Oncogene Proteins / genetics
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Oncogene Proteins / metabolism*
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Signal Transduction
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Transcription Factors / genetics
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Transcription Factors / metabolism*
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Tumor Microenvironment
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / metabolism
Substances
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Oncogene Proteins
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Transcription Factors
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Tumor Suppressor Protein p53