Nasopharyngeal carcinoma (NPC) is a malignant tumor with high metastatic features originating from the nasopharynx. However, the underlying mechanism of Suppressor of variegation 3–9 homolog 2 (SUV39H2) in NPC remains poorly understood. RT‐qPCR was carried out to examine SUV39H2 and SIRT1 expression in NPC tissues and cells. Kaplan–Meier method was utilized to evaluate the association between SUV39H2 level and overall survival. The function of SUV39H2 and SIRT1 in NPC cell viability, metastasis, and apoptosis was tested through CCK‐8, transwell, and flow cytometry experiments. Here, it was uncovered that SUV39H2 level was augmented in NPC tissues and cells. Moreover, SUV39H2 expedited NPC cell viability, metastasis, and inhibited apoptosis, while SIRT1 addition reversed these impacts. Besides, SUV39H2 induced H3K9me3 enhancement to repress SIRT1 transcription via binding to SIRT1 promoter. Collectively, our results demonstrated upregulated SUV39H2 aggravated NPC tumorigenesis through SIRT1, which may offer a potential therapeutic target for NPC.

中文翻译：

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组蛋白甲基转移酶 SUV39H2 通过调节 SIRT1 支持鼻咽癌细胞转移


鼻咽癌 （NPC） 是一种起源于鼻咽部的具有高度转移特征的恶性肿瘤。然而，NPC 中杂色 3-9 同源物 2 （SUV39H2） 抑制因子的潜在机制仍然知之甚少。进行 RT-qPCR 以检测 NPC 组织和细胞中 SUV39H2 和 SIRT1 的表达。采用 Kaplan-Meier 方法评估 SUV39H2 水平与总生存期之间的相关性。通过 CCK-8 、 transwell 和流式细胞术实验检测 SUV39H2 和 SIRT1 在 NPC 细胞活力、转移和凋亡中的功能。在这里，发现 NPC 组织和细胞中的 SUV39H2 水平增加。此外，SUV39H2 加速了 NPC 细胞活力、转移并抑制了细胞凋亡，而 SIRT1 的添加则逆转了这些影响。此外，SUV39H2 通过与 SIRT1 启动子结合诱导 H3K9me3 增强以抑制 SIRT1 转录。总的来说，我们的结果表明 SIRT1 上调SUV39H2加重了 NPC 肿瘤发生，这可能为 NPC 提供了潜在的治疗靶点。