EZH2,多梳抑制复合物2(PRC2)的亚基,是一种重要的甲基转移酶,可催化赖氨酸27处组蛋白H3(H3K27me3)的三甲基化。EZH2在各种恶性肿瘤中过表达。这里,我们研究了ATLL和其他T细胞肿瘤中EZH2的表达和与EZH2表达相关的潜在信号分子.EZH2、pERK、MYC,和pSTAT3对43例ATLL和104例其他T细胞肿瘤的影响。对ATLL病例的Ki-67、SUZ12和H3K27me3进行了进一步的IHC研究。所有ATLL病例均显示EZH2过表达。在其他T细胞肿瘤中,EZH2过表达的高患病率(86%),除了T-PLL(33%)。在ATLL,EZH2过表达与pERK共表达相关(86%),而只有一小部分病例显示MYC(7%)或pSTAT3(14%)共表达。在其他T细胞肿瘤中,有一个变量,但更高,EZH2与pERK共表达,MYC,和STAT3。在ATLL,增强的EZH2表达与较高的Ki-67染色相关,SUZ12(另一个PRC2亚基),和H3K27me3共表达。总之,EZH2在ATLL中过表达并与pERK表达相关。它与增加的增殖指数相关,表明积极的临床过程。EZH2还与SUZ12和H3K27me3共表达相关,通过三甲基化表明其PRC2依赖性催化活性。此外,EZH2在大多数T细胞肿瘤中过度表达,这表明EZH2在T细胞肿瘤发生中可能是一种致癌蛋白。EZH2和pERK可以作为治疗侵袭性ATLL的潜在治疗靶点。EZH2也可以靶向其他T细胞肿瘤。
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.