Epigenetics helps define current cell states, yet also shapes how cells respond to external cues such as differentiation or stress. The epigenetic plasticity of a cell describes how flexible this regulation is. Early embryonic cells are highly plastic in that they can generate all adult cell types. As development progresses, this plasticity is lost as normal healthy adult cells are locked in their identity. Crucially, aberrant reactivation may contribute to pathologies such as cancer.
The epigenetic plasticity of cells is tightly controlled and regulated in part by epigenetic priming factors. These establish a permissive epigenetic landscape to enable future transcriptional changes. Epigenetic priming factors are frequently mis-regulated in cancers, potentially increasing their epigenetic plasticity and contributing to tumorigenesis. However, we know little of the identity of epigenetic priming factors and their mode of action. We are now exploring how these important gatekeepers of early embryonic cell fate transitions may be hijacked in cancers to promote cell plasticity and facilitate acquisition of new identities and functions. By discovering the principles driving epigenetic plasticity in development, we can further our understanding of how this goes awry in cancer, leading to new areas for therapeutic intervention.