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首页> 外文期刊>Oncology reports >SET and MYND domain-containing protein 3 is overexpressed in human glioma and contributes to tumorigenicity
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SET and MYND domain-containing protein 3 is overexpressed in human glioma and contributes to tumorigenicity

机译：包含SET和MYND结构域的蛋白3在人脑胶质瘤中过表达，并有助于致瘤性

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SET and MYND domain-containing protein 3 (SMYD3) is a histone H3 lysine 4 (H3K4) di- and tri-methyltransferase that forms a transcriptional complex with RNA polymerase II and plays an important role in early embryonic lineage commitment through the activation of lineage-specific genes. SMYD3 activates the transcription of oncogenes and cell cycle genes in gastric and breast cancer cells. However, the contribution of SMYD3 in glioma tumorigenesis remains unknown. Here, we determined the expression of SMYD3 and assessed its clinical significance in human glioma. We found that SMYD3 was overexpressed in human glioma but not in normal brain tissue. The level of SMYD3 protein expression in human glioma tissues was directly correlated with the glioma grade. The level of SMYD3 protein expression in human glioma tissues was inversely correlated with patient survival. Enforced SMYD3 expression promoted glioma LN-18 cell proliferation. Inhibition of SMYD3 expression in glioma T98G cells suppressed their anchorage-independent growth in vitro and tumorigenicity in vivo. Furthermore, we found that SMYD3 regulated the expression of p53 protein, which is essential in SMYD3-induced cell growth in glioma cells. These results showed that SMYD3 is overexpressed in human glioma and contributes to glioma tumorigenicity through p53. Therefore, SMYD3 may be a new potential therapeutic target for human malignant glioma.
机译：包含SET和MYND域的蛋白质3（SMYD3）是组蛋白H3赖氨酸4（H3K4）二甲基和三甲基转移酶，与RNA聚合酶II形成转录复合物，并通过激活谱系在早期胚胎谱系的定型中起重要作用特异性基因。 SMYD3激活胃癌和乳腺癌细胞中癌基因和细胞周期基因的转录。但是，SMYD3在神经胶质瘤肿瘤发生中的作用仍然未知。在这里，我们确定了SMYD3的表达并评估了其在人脑胶质瘤中的临床意义。我们发现SMYD3在人类神经胶质瘤中过表达，但在正常脑组织中却未过表达。人神经胶质瘤组织中SMYD3蛋白表达水平与神经胶质瘤等级直接相关。人脑胶质瘤组织中SMYD3蛋白表达水平与患者生存率呈负相关。增强的SMYD3表达促进神经胶质瘤LN-18细胞增殖。胶质瘤T98G细胞中SMYD3表达的抑制抑制了它们在体外的不依赖锚定的生长和体内的致瘤性。此外，我们发现SMYD3调节p53蛋白的表达，这在SMYD3诱导的神经胶质瘤细胞生长中至关重要。这些结果表明，SMYD3在人神经胶质瘤中过表达，并通过p53促进神经胶质瘤的致瘤性。因此，SMYD3可能是人类恶性神经胶质瘤的新潜在治疗靶点。

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