增强子是决定细胞特性和肿瘤进展的必不可少的顺式作用调控元件。增强子的功能取决于其与靶基因启动子在局部染色质环境内的物理相互作用。增强子再编程是癌症发病机制中重要的一环，可以由顺式和反式因子推动。在许多癌症类型中，超级增强子会在致癌基因处获得，并且代表了癌症治疗的潜在靶点。BET和CDK抑制剂通过增强子功能机制发挥作用，并在多种癌症疗法中显示出有希望的结果。基因组编辑是癌症治疗中重新编程增强子的另一种方法。过去几年中，多位作者对增强子与癌症的关系进行了修订，主要关注增强子对癌症的影响机制。在此，我们强调超级增强子在癌症发病机制中的作用以及涉及表观遗传调控因子（BETi和CDKi）的新疗法。我们建议了解其活性机制将有助于这些抗癌药物的临床成功。

Enhancers are essential cis-acting regulatory elements that determine cell identity and tumor progression. Enhancer function is dependent on the physical interaction between the enhancer and its target promoter inside its local chromatin environment. Enhancer reprogramming is an important mechanism in cancer pathogenesis and can be driven by both cis and trans factors. Super enhancers are acquired at oncogenes in numerous cancer types and represent potential targets for cancer treatment. BET and CDK inhibitors act through mechanisms of enhancer function and have shown promising results in therapy for various types of cancer. Genome editing is another way to reprogram enhancers in cancer treatment. The relationship between enhancers and cancer has been revised by several authors in the past few years, which mainly focuses on the mechanisms by which enhancers can impact cancer. Here, we emphasize SE's role in cancer pathogenesis and the new therapies involving epigenetic regulators (BETi and CDKi). We suggest that understanding mechanisms of activity would aid clinical success for these anti-cancer agents.