Title: Somatic Pluripotent Genes in Tissue Re- pair, Developmental Disease, and Cancer

  • Hannah Wollenzien Genetics and Genomics Group, Cellular Therapies and Stem Cell Biology Group, and the Cancer Biology and Immunotherapies Group, Sanford Research, 2301 East 60th Street North, Sioux Falls, SD 57104, USA.
    Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, 414 E. Clark St. Vermillion, SD 57069, USA.
  • Ellen Voigt Genetics and Genomics Group, Cellular Therapies and Stem Cell Biology Group, and the Cancer Biology and Immunotherapies Group, Sanford Research, 2301 East 60th Street North, Sioux Falls, SD 57104, USA.
  • Michael S. Kareta Genetics and Genomics Group, Cellular Therapies and Stem Cell Biology Group, and the Cancer Biology and Immunotherapies Group, Sanford Research, 2301 East 60th Street North, Sioux Falls, SD 57104, USA.
    Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, 414 E. Clark St. Vermillion, SD 57069, USA.
    Department of Pediatrics, Sanford School of Medicine, 1400 W. 22nd St., Sioux Falls, SD 57105, USA.
    Department of Chemistry and Biochemistry, South Dakota State University, 1175 Medary Ave, Brookings, SD 57006, USA.

Abstract

Embryonic stem cells possess the ability to differentiate into all cell types of the body. This pliable developmental state is achieved by the function of a series of pluripotency factors, classically identified as OCT4, SOX2, and NANOG. These pluripotency factors are responsible for activating the larger pluripotency networks and the self-renewal programs which give ES cells their unique characteristics. However, during differentiation pluripotency networks become downregulated as cells achieve greater lineage specification and exit the cell cycle. Typically the repression of plu-ripotency is viewed as a positive factor to ensure the fidelity of cellular identity by restricting cellular pliancy. Consistent with this view, the expression of pluripotency factors is greatly restricted in somatic cells. However, there are examples whereby cells either maintain or reactivate pluripotency factors to preserve the increased potential for the healing of wounds or tissue homeostasis. Additionally there are many examples where these pluripotency factors become reactivated in a variety of human pathologies, particularly cancer. In this review, we will summarize the somatic repression of pluripotency factors, their role in tissue homeostasis and wound repair, and the human diseases that are associated with pluripotency factor misregulation with an emphasis on their role in the etiology of multiple cancers.

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Published
2018-10-28
Citation
Kareta M. et al. (2018) Somatic Pluripotent Genes in Tissue Re-pair, Developmental Disease, and Cancer Science Publishing Group Journal 1(2).
Corresponding author

Michael S. Kareta
Email: michael.kareta@sanfordhealth.org

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