【摘要】 癌基因激活和抑癌基因失活被视为驱动肿瘤的核心事件，而近年研究发现，表观遗传重塑也参与了这一调控肿瘤发生发展的重要过程。众多证据表明，癌症相关基因的变异能够改变细胞内多种表观修饰状态。本文重点阐述了TP53、PTEN、IDH1等抑癌基因及BRAF、KRAS、MYC等原癌基因的异常调控通过改变DNA甲基化、组蛋白修饰、染色质重塑、非编码RNA调控等表观遗传状态，进而驱动肿瘤异质性、可塑性及耐药性的调控机制。这些研究表明，癌症相关基因不仅能够作用于下游的表观调控因子导致表观重塑，同时表观异常调控也可通过反馈回路主动参与肿瘤演进。据此，本文系统总结了基因变异驱动癌症过程中与异常表观遗传调控相关的关键分子机制，旨为深入理解表观重塑在基因变异推动肿瘤演进中的生物学意义，并为靶向肿瘤中表观遗传相关靶点的治疗策略提供参考。更多还原

【Abstract】 Oncogene activation and tumor suppressor gene inactivation have long been recognized as core genetic events driving tumorigenesis. Recent studies, however, have revealed that epigenetic remodeling extensively participates in the regulation of cancer development. Emerging evidence indicates that alterations in cancer genes can modify various epigenetic states within cells. This review focuses on how aberrant regulation of key tumor suppressors—including TP53(tumor protein p53, TP53), PTEN(phosphatase and tensin homolog, PTEN), and IDH1(isocitrate dehydrogenase 1, IDH1)—and proto-oncogenes—such as BRAF(B-Raf proto-oncogene, BRAF), KRAS(Kirsten rat sarcoma viral oncogene homolog, KRAS), and MYC(MYC proto-oncogene, MYC)—orchestrate epigenetic reprogramming via alterations in DNA methylation, histone modifications, chromatin remodeling, and non-coding RNA regulation, thereby driving tumor heterogeneity, plasticity, and drug resistance. Accumulating evidence indicates that epigenetic regulation not only serves as a downstream executor of genetic alterations, but also actively participates in tumor evolution through feedback loops. By summarizing the intricate crosstalk between oncogenic signaling and epigenetic machinery, this review aims to advance the understanding of the biological significance of oncogenes in cancer progression and therapy, and to provide a theoretical foundation for developing therapeutic strategies that target tumor epigenetic plasticity.更多还原