Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
Int Rev Cell Mol Biol. 2024;387:1-25. doi: 10.1016/bs.ircmb.2024.05.003. Epub 2024 Jun 19.
Epigenetics has transformed our understanding of cancer by revealing how changes in gene activity, which do not alter the DNA itself, can initiate and progress the disease. These changes include adjustments in DNA methylation, histone configuration, and non-coding RNA activity. For instance, DNA methylation can inactivate genes that typically protect against cancer, leading to broader genomic instability. Histone modifications can alter how tightly DNA is wound, influencing which genes are active or silenced; while non-coding RNAs can interfere with the messages that direct protein production, impacting cancer-related processes. Unlike genetic mutations, which are permanent and irreversible, epigenetic changes provide a malleable target for therapeutic intervention, allowing potentially reversible adjustments to gene expression patterns. This flexibility is essential in the complex landscape of cancer where static genetic solutions may be insufficient. Additionally, epigenetics bridges the gap between genetic predispositions and environmental influences on cancer, offering a comprehensive framework for understanding how lifestyle factors and external exposures impact cancer risk and progression. The integration of epigenetics into cancer research not only enhances our understanding of the disease but also opens innovative avenues for intervention that were previously unexplored in traditional genetic-focused studies. Technologies like advanced sequencing and precise epigenetic modification are paving the way for early cancer detection and more personalized treatment approaches, highlighting the critical role of epigenetics in modern cancer care.
表观遗传学通过揭示基因活性的变化如何引发和推进疾病,改变了我们对癌症的认识。这些变化包括 DNA 甲基化、组蛋白结构和非编码 RNA 活性的调整。例如,DNA 甲基化可以使通常能预防癌症的基因失活,导致更广泛的基因组不稳定。组蛋白修饰可以改变 DNA 的缠绕程度,影响哪些基因是活跃的或沉默的;而非编码 RNA 可以干扰指导蛋白质产生的信息,影响与癌症相关的过程。与遗传突变不同,遗传突变是永久性和不可逆转的,表观遗传变化为治疗干预提供了一个可塑的靶点,允许对基因表达模式进行潜在的可逆调整。这种灵活性在癌症这个复杂的领域中至关重要,因为静态的遗传解决方案可能不够充分。此外,表观遗传学弥合了遗传倾向和环境对癌症影响之间的差距,为理解生活方式因素和外部暴露如何影响癌症风险和进展提供了一个全面的框架。将表观遗传学纳入癌症研究不仅增强了我们对疾病的理解,还为以前在传统以遗传为重点的研究中未探索过的干预提供了创新途径。高级测序和精确的表观遗传修饰等技术为早期癌症检测和更个性化的治疗方法铺平了道路,突显了表观遗传学在现代癌症治疗中的关键作用。