Abstract
The physiological properties of pluripotency in stem cells and the processes of cell specialization are governed by epigenetic mechanisms, as they are inheritable but not dependent on the cell genotype. There is cumulating evidence demonstrating the presence of cells with stem cell properties within tumors, suggesting that these cells are responsible for tumor growth and heterogeneity. As epigenetic control of self-renewal and pluripotency is a hallmark of stem cells, there is increased interest in studying similar epigenetic mechanisms governing these stemness properties in cancer stem cells. Here we will review the evidence supporting a role for epigenetic mechanisms in the induction of cancer stem cells, with an emphasis on the epigenetic regulatory networks involved in the establishment of normal self-renewal and pluripotency, and their potential deregulation in cancer. We will also discuss the data supporting the plasticity of these mechanisms and its potential therapeutic implications.
Acknowledgments
We apologize to colleagues whose relevant works were not cited owing to space limitations. We gratefully acknowledge A Paliwal for critical reading of the manuscript.
Financial & competing interests disclosure
The work in the IARC Epigenetics Group is supported by grants from the National Institutes of Health/National Cancer Institute (NIH/NCI), United States; the Association pour la Recherche sur le Cancer (ARC), France; la Ligue Nationale (Française) Contre le Cancer, France; the European Network of Excellence Environmental Cancer Risk, Nutrition and Individual Susceptibility (ECNIS), and Agence Nationale de Recherhe Contre le Sida et Hépatites Virales (ANRS, France), and the Swiss Bridge Award. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.