Abstract：
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.
摘要：
鼻咽癌（NPC）是一种具有高度转移特征的恶性肿瘤，起源于鼻咽。然而,在NPC中抑制杂色3-9同源物2（SUV39H2）的潜在机制仍然知之甚少。进行RT-qPCR以检测SUV39H2和SIRT1在NPC组织和细胞中的表达。使用Kaplan-Meier方法评估SUV39H2水平与总生存期之间的关联。SUV39H2和SIRT1在鼻咽癌细胞活力中的作用,转移,通过CCK-8，transwell，和流式细胞术实验。这里,发现NPC组织和细胞中SUV39H2水平升高。此外，SUV39H2加速NPC细胞活力，转移,抑制细胞凋亡，而SIRT1的添加逆转了这些影响。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，我们的结果表明上调的SUV39H2通过SIRT1加重了NPC肿瘤发生,这可能为NPC提供一个潜在的治疗靶点.
