通讯作者: 许树才, 2319125047@qq.com

DOI：10.12201/bmr.202603.00092

Research progress on the anti-tumor effect of traditional Chinese medicine based on epigenetic mechanisms

• 摘要：肿瘤是全球范围内导致人类死亡的主要疾病之一,其临床治疗手段有限,容易出现耐药性,且治愈率普遍偏低,而表观遗传调控作为肿瘤发生的核心机制之一,以DNA甲基化失衡、组蛋白修饰紊乱和非编码RNA失调为特征,其可逆性为肿瘤治疗提供了全新靶点。近年来,中医药通过多成分、多靶点特性调控表观遗传抑制肿瘤的研究备受关注。例如中药有效成分(如姜黄素)可直接靶向DNA甲基转移酶(DNMTs)、组蛋白去乙酰化酶(HDACs)等关键酶,恢复抑癌基因表达。文章系统综述中医药调控表观遗传抑制肿瘤的多维度机制(DNA甲基化、组蛋白修饰、非编码RNA),总结临床转化进展,并针对机制深度不足、质量控制薄弱等挑战提出展望,旨在为中西医结合治疗肿瘤提供理论支撑与新策略。

  关键词： 中医药; 表观遗传; 肿瘤; DNA甲基化; 组蛋白修饰; 非编码RNA

   

  Abstract: Tumors are one of the leading causes of human mortality worldwide, with limited clinical treatment options, a high propensity for drug resistance, and generally low cure rates. Epigenetic regulation, as a core mechanism in tumorigenesis, is characterized by imbalances in DNA methylation, disruptions in histone modifications, and dysregulation of non-coding RNAs. Its reversibility offers novel targets for cancer therapy. In recent years, traditional Chinese medicine (TCM) has garnered significant attention for its ability to modulate epigenetic mechanisms and inhibit tumors through its multi-component, multi-target characteristics. For example, active components of TCM, such as curcumin, can directly target key enzymes like DNA methyltransferases (DNMTs) and histone deacetylases (HDACs), thereby restoring the expression of tumor suppressor genes. This article systematically reviews the multi-dimensional mechanisms by which TCM regulates epigenetics to suppress tumors (including DNA methylation, histone modifications, and non-coding RNAs), summarizes the progress in clinical translation, and addresses challenges such as insufficient mechanistic depth and weak quality control. The aim is to provide theoretical support and new strategies for integrated traditional Chinese and Western medicine in cancer treatment.

  Key words: Traditional Chinese medicine; Epigenetics; Tumors; DNA methylation; Histone modification; Non-coding RNAs.

  提交时间：2026-03-20

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• 序号	提交日期	编号	操作
  1	2026-02-24	10.12201/bmr.202603.00092V1	下载

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