The histone demethylase KDM6B, also known as jumonji domain-containing protein 3 (JMJD3), is an epigenetic regulator which plays important roles in immune activation, tissue regeneration, cellular senescence and cancer metastasis. But, the role of KDM6B in glioma metastasis is poorly understood. In this study, we achieved transcriptional regulation of KDM6B in glioma cells using CRISPR interference (CRISPRi) and CRISPR activation (CRISPRa). Our results showed that KDM6B promotes the proliferation, migration and invasion of human glioblastoma cells U87 and U251 using CCK8, scratch and transwell assays. Further results indicated that KDM6B increases the expression of SNAI1, a key factor of epithelial-mesenchymal transition (EMT). KDM6B catalyzes the demethylation of histone H3 Lys 27 trimethylation (H3K27me3) in the promoter of SNAI1, which is important for SNAI1 upregulation. Taken together, these findings provide new insight into the mechanism by which KDM6B promotes glioma metastasis.

中文翻译：

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组蛋白H3 Lys 27脱甲基酶KDM6B部分地通过调节SNAI1的表达来促进神经胶质瘤细胞的迁移和侵袭。

组蛋白脱甲基酶KDM6B，也称为含jumonji域的蛋白质3（JMJD3），是一种表观遗传调节剂，在免疫激活，组织再生，细胞衰老和癌症转移中起重要作用。但是，对KDM6B在神经胶质瘤转移中的作用了解甚少。在这项研究中，我们使用CRISPR干扰（CRISPRi）和CRISPR激活（CRISPRa）实现了神经胶质瘤细胞中KDM6B的转录调控。我们的结果表明，使用CCK8，刮擦和Transwell分析，KDM6B促进人胶质母细胞瘤细胞U87和U251的增殖，迁移和侵袭。进一步的结果表明，KDM6B增加了SNAI1的表达，SNAI1是上皮-间质转化（EMT）的关键因素。KDM6B在SNAI1启动子中催化组蛋白H3 Lys 27 trimethylation（H3K27me3）的去甲基化，这对于SNAI1上调很重要。综上所述，这些发现为KDM6B促进神经胶质瘤转移的机制提供了新的见解。