肺癌（LC）的发病机制是一个多方面的过程，受多种因素影响。除了基因突变和环境影响之外，越来越多的证据表明表观遗传机制在 LC 的发生和进展中发挥着重要作用。 Polycomb 抑制复合物 2 (PRC2) 由 EZH1/2、SUZ12 和 EED 组成，是一种表观遗传沉默子，控制靶基因的表达，对多细胞生物体的细胞身份至关重要。 PRC2 的异常表达已被证明可通过多种途径促进 LC 的进展。尽管靶向抑制 EZH2 已被证明具有延缓 LC 进展和提高化疗敏感性的潜力，但 PRC2 酶抑制剂在 LC 中的有效性有限，因此有必要更全面地了解 PRC2 的作用。本文综述了PRC2的核心亚基及其相互作用，并概述了PRC2在癌症中异常表达的机制及其在肿瘤免疫中的作用。我们还总结了 PRC2 在调节 LC 细胞中上皮间质转化、侵袭性转移、细胞凋亡、细胞周期调节、自噬和 PRC2 介导的 LC 化疗药物耐药等生物学行为中的重要作用。最后，我们探讨了针对 PRC2 的药物研究和评估的最新突破，以及这些药物治疗多种人类癌症疗效的临床研究的最新结果。版权所有 © 2023 高，李，曹，刘、陈、康。

The pathogenesis of lung cancer (LC) is a multifaceted process that is influenced by a variety of factors. Alongside genetic mutations and environmental influences, there is increasing evidence that epigenetic mechanisms play a significant role in the development and progression of LC. The Polycomb repressive complex 2 (PRC2), composed of EZH1/2, SUZ12, and EED, is an epigenetic silencer that controls the expression of target genes and is crucial for cell identity in multicellular organisms. Abnormal expression of PRC2 has been shown to contribute to the progression of LC through several pathways. Although targeted inhibition of EZH2 has demonstrated potential in delaying the progression of LC and improving chemotherapy sensitivity, the effectiveness of enzymatic inhibitors of PRC2 in LC is limited, and a more comprehensive understanding of PRC2's role is necessary. This paper reviews the core subunits of PRC2 and their interactions, and outlines the mechanisms of aberrant PRC2 expression in cancer and its role in tumor immunity. We also summarize the important role of PRC2 in regulating biological behaviors such as epithelial mesenchymal transition, invasive metastasis, apoptosis, cell cycle regulation, autophagy, and PRC2-mediated resistance to LC chemotherapeutic agents in LC cells. Lastly, we explored the latest breakthroughs in the research and evaluation of medications that target PRC2, as well as the latest findings from clinical studies investigating the efficacy of these drugs in the treatment of various human cancers.Copyright © 2023 Gao, Li, Cao, Liu, Chen and Kang.