Enhancer of Zeste Homolog 1 (EZH1) and Enhancer of Zeste Homolog 2 (EZH2) are the key components of polycomb repressive complex 2 (PRC2); however, the roles of these proteins in oral squamous cell carcinoma (OSCC) have yet to be elucidated. In this study, we aimed to determine the respective roles of these proteins in OSCC by investigating the expression levels of EZH1 and EZH2 in OSCC tissues (N = 63) by immunohistochemistry. In addition, we used lentiviruses to construct stable OSCC cell lines that overexpressed EZH1 and EZH2. Then, we investigated these cell lines for cell viability, colony formation capacity, stemness, and epithelial-mesenchymal transition (EMT). Binding competition between EZH1 and EZH2 with PRC2 was further evaluated using Co-immunoprecipitation (Co-IP). Compared with normal tissues, the expression levels of EZH2 in OSCC tissues was up-regulated, while the expression of EZH1 was down-regulated. EZH2 enhanced cell viability, colony formation capacity, stemness, and EMT, while EZH1 did not. Furthermore, analysis indicated that EZH1 and EZH2 bound competitively to PRC2 and influenced the methylation status of H3K27. In conclusion, our findings verified that EZH1 and EZH2 play opposing roles in OSCC and that EZH1 and EZH2 compete as the key component of PRC2, thus affecting the characteristics of OSCC via the methylation of H3K27.

中文翻译：

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EZH1和EZH2促进口腔鳞癌发生的竞争机制

增强子 Zeste 同源物 1 (EZH1) 和增强子 Zeste 同源物 2 (EZH2) 是多梳抑制复合物 2 (PRC2) 的关键成分；然而，这些蛋白质在口腔鳞状细胞癌（OSCC）中的作用尚未阐明。在本研究中，我们旨在通过免疫组织化学研究 OSCC 组织（N = 63）中 EZH1 和 EZH2 的表达水平来确定这些蛋白在 OSCC 中各自的作用。此外，我们使用慢病毒构建了过表达 EZH1 和 EZH2 的稳定 OSCC 细胞系。然后，我们研究了这些细胞系的细胞活力、集落形成能力、干性和上皮间质转化（EMT）。使用免疫共沉淀 (Co-IP) 进一步评估 EZH1 和 EZH2 与 PRC2 之间的结合竞争。与正常组织相比,OSCC组织中EZH2的表达水平上调,而EZH1的表达水平下调。EZH2 增强细胞活力、集落形成能力、干性和 EMT，而 EZH1 则不然。此外，分析表明EZH1和EZH2竞争性地结合PRC2并影响H3K27的甲基化状态。总之，我们的研究结果证实，EZH1 和 EZH2 在 OSCC 中发挥相反的作用，并且 EZH1 和 EZH2 竞争作为 PRC2 的关键组成部分，从而通过 H3K27 的甲基化影响 OSCC 的特征。