Abstract
Cellular plasticity in prostate cancer promotes treatment resistance. Several independent studies have used mouse models, single-cell RNA sequencing, and genetic lineage tracing approaches to characterize cellular differentiation and plasticity during prostate organogenesis, homeostasis and androgen-mediated tissue regeneration. We review these findings and recent work using immune-competent genetically-engineered mouse models to characterize cellular plasticity and clonal dynamic changes during prostate cancer progression. Collectively these studies highlight the influence of the tumor microenvironment and the function of epigenetic regulators in promoting cellular plasticity. How the epigenetic alternations that promote cell plasticity affect tumor immunogenicity remains an active area of research with implications for disease treatment.