EZH2, a subunit of the polycomb repressive complex 2 (PRC2), is an important methyltransferase that catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3). EZH2 is overexpressed in various malignancies. Here, we investigated EZH2 expression and potential signaling molecules that correlate with EZH2 expression in ATLL and other T-cell neoplasms. Immunohistochemical staining (IHC) was performed for EZH2, pERK, MYC, and pSTAT3 on 43 ATLL cases and 104 cases of other T-cell neoplasms. Further IHC studies were conducted for Ki-67, SUZ12, and H3K27me3 on ATLL cases. All ATLL cases showed EZH2 overexpression. In other T-cell neoplasms, a high prevalence of EZH2 overexpression was identified (86%), except for T-PLL (33%). In ATLL, EZH2 overexpression correlated with pERK co-expression (86%), while only a small subset of cases showed MYC (7%) or pSTAT3 (14%) co-expression. In the other T-cell neoplasms, there was a variable, but higher, co-expression of EZH2 with pERK, MYC, and pSTAT3. In ATLL, enhanced EZH2 expression correlated with higher Ki-67 staining, SUZ12 (another PRC2 subunit), and H3K27me3 co-expression. In conclusion, EZH2 is overexpressed in ATLL and is associated with pERK expression. It correlates with an increased proliferation index, indicating an aggressive clinical course. EZH2 also correlates with SUZ12 and H3K27me3 co-expression, suggesting its PRC2-dependent catalytic activity through trimethylation. Additionally, EZH2 is overexpressed in most T-cell neoplasms, suggesting that EZH2 could function as an oncogenic protein in T-cell tumorigenesis. EZH2 and pERK could serve as potential therapeutic targets for treating aggressive ATLL. EZH2 could also be targeted in other T-cell neoplasms.
EZH2是多梳抑制复合体2（PRC2）的一个亚基，是一种重要的甲基转移酶，负责催化组蛋白H3第27位赖氨酸的三甲基化（H3K27me3）。EZH2在多种恶性肿瘤中过度表达。本研究探讨了EZH2在成人T细胞白血病/淋巴瘤（ATLL）及其他T细胞肿瘤中的表达情况，以及与EZH2表达相关的潜在信号分子。我们对43例ATLL和104例其他T细胞肿瘤进行了EZH2、pERK、MYC和pSTAT3的免疫组织化学染色。此外，对ATLL病例还进行了Ki-67、SUZ12和H3K27me3的进一步免疫组化研究。所有ATLL病例均显示EZH2过度表达。在其他T细胞肿瘤中，除T-PLL（33%）外，EZH2过度表达的比例也很高（86%）。在ATLL中，EZH2过度表达与pERK共表达相关（86%），而仅有少数病例显示MYC（7%）或pSTAT3（14%）共表达。在其他T细胞肿瘤中，EZH2与pERK、MYC和pSTAT3的共表达程度不一，但总体较高。在ATLL中，EZH2表达增强与较高的Ki-67染色、SUZ12（PRC2的另一亚基）和H3K27me3共表达相关。总之，EZH2在ATLL中过度表达，并与pERK表达相关。它与增殖指数升高相关，表明其临床病程具有侵袭性。EZH2还与SUZ12和H3K27me3共表达相关，提示其通过三甲基化发挥PRC2依赖的催化活性。此外，EZH2在大多数T细胞肿瘤中过度表达，表明EZH2可能在T细胞肿瘤发生中发挥致癌蛋白的作用。EZH2和pERK可能成为治疗侵袭性ATLL的潜在治疗靶点。EZH2也可能成为其他T细胞肿瘤的治疗靶点。
肿瘤(癌症)患者之家