Epigenetic regulators are one of the most commonly mutated classes of genes in cancer. During cancer initiation, mutated epigenetic regulators lead to oncogenic cellular reprogramming and promote the acquisition of uncontrolled self-renewal. The emergence of CSCs requires elaborate reorganization of the epigenome.
During cancer growth, epigenetic mechanisms integrate the effect of cell-intrinsic (i.e., subclonal mutations) and cell-extrinsic (i.e., signaling from the microenvironment) changes and establish intratumoral heterogeneity, either promoting or inhibiting the CSC state.
‘Loose’ epigenetic constraints in cancer cells enhance cellular plasticity and allow reversible transitions between different phenotypic states. Enhanced cellular plasticity favors cancer cell adaptability and resistance to therapy.
Modulation of epigenetic processes allows targeting of the most downstream determinants of the CSC state
