Mediators of induced pluripotency and their role in cancer cells – current scientific knowledge and future perspectives

Authors

  • Mathias Bernhardt,

    1. Skin Cancer Unit, German Cancer Research Center (DKFZ), Heidelberg, Germany
    2. Department of Dermatology, Venereology and Allergology, University Medical Center Mannheim, Ruprecht-Karl University of Heidelberg, Mannheim, Germany
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  • Marta Galach,

    1. Skin Cancer Unit, German Cancer Research Center (DKFZ), Heidelberg, Germany
    2. Department of Dermatology, Venereology and Allergology, University Medical Center Mannheim, Ruprecht-Karl University of Heidelberg, Mannheim, Germany
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  • Daniel Novak,

    1. Skin Cancer Unit, German Cancer Research Center (DKFZ), Heidelberg, Germany
    2. Department of Dermatology, Venereology and Allergology, University Medical Center Mannheim, Ruprecht-Karl University of Heidelberg, Mannheim, Germany
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  • Dr. Jochen Utikal

    Corresponding author
    1. Skin Cancer Unit, German Cancer Research Center (DKFZ), Heidelberg, Germany
    2. Department of Dermatology, Venereology and Allergology, University Medical Center Mannheim, Ruprecht-Karl University of Heidelberg, Mannheim, Germany
    • Department of Dermatology, Venereology and Allergology, University Medical Center Mannheim, Ruprecht-Karl University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68135 Mannheim, Germany
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Abstract

The discovery that overexpression of the transcription factors Oct4, Sox2, Klf4 and c-Myc reprograms differentiated cells into “induced pluripotent stem cells” (iPSCs) has extended our understanding of mechanisms required to maintain stem cell pluripotency and to drive differentiation. Subsequently, additional factors have been discovered that are able to induce a pluripotent state. Recently several groups have succeeded in reprogramming cancer cells to iPSC-like induced pluripotent cancer cells by use of the method established for the generation of iPSCs. This discovery highlighted several striking similarities between pluripotent stem cells and cancer cells, in turn implying that tumorigenesis and reprogramming are partly promoted by overlapping mechanisms. Thus, research on reprogramming might help unravel the mechanisms of carcinogenesis, and vice versa. This review gives an overview of the common features of pluripotent stem cells and cancer cells and summarizes the present state of knowledge in the field of cancer cell reprogramming.

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