Williams Emily C, Shibata Maho
Department of Anatomy and Cell Biology, The George Washington University School of Medicine and Health Sciences, Washington, DC, USA; The George Washington University Cancer Center, The George Washington University School of Medicine and Health Sciences, Washington, DC, USA.
Department of Anatomy and Cell Biology, The George Washington University School of Medicine and Health Sciences, Washington, DC, USA; The George Washington University Cancer Center, The George Washington University School of Medicine and Health Sciences, Washington, DC, USA.
Cancer Lett. 2024 Dec 25;611:217430. doi: 10.1016/j.canlet.2024.217430.
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.
前列腺癌中的细胞可塑性会促进治疗抗性。多项独立研究已使用小鼠模型、单细胞RNA测序和遗传谱系追踪方法，来表征前列腺器官发生、内稳态以及雄激素介导的组织再生过程中的细胞分化和可塑性。我们回顾了这些发现以及近期利用具有免疫活性的基因工程小鼠模型开展的研究工作，以表征前列腺癌进展过程中的细胞可塑性和克隆动态变化。这些研究共同强调了肿瘤微环境的影响以及表观遗传调节因子在促进细胞可塑性方面的作用。促进细胞可塑性的表观遗传改变如何影响肿瘤免疫原性仍是一个活跃的研究领域，对疾病治疗具有重要意义。
