低级别胶质瘤（LGG）是成年人第二常见的脑恶性肿瘤，严重威胁患者健康并有高复发率。组蛋白H3/H4伴侣抗沉默功能1B（ASF1B）与肿瘤的启动和发展紧密相关。讨论了ASF1B在LGG中的表达和调节机制。GEPIA数据库预测了LGG患者中ASF1B的表达以及ASF1B与LGG患者的总生存率和无病生存率的关联。TCGA数据库研究了ASF1B在LGG患者中的独立预后价值。采用RT-qPCR和Western blot评估了LGG细胞系中ASF1B的表达。抑制ASF1B表达后，CCK8和集落形成实验评估细胞增殖。流式细胞术分析和TUNEL实验评估细胞周期和凋亡。创口愈合和转移实验测量细胞迁移和侵袭能力。西方印迹测试增殖、周期、凋亡和转移相关蛋白的表达。STRING和GeneMANIA数据库预测了ASF1B和发缭样激酶1（TLK1）之间的关系。ChIP实验证实了ASF1B与TLK1的亲和力。随后，过度表达TLK1并干扰ASF1B表达，执行功能实验。发现ASF1B在LGG组织和细胞中增加，提示LGG患者预后不良。ASF1B不是LGG的独立预后因素。ASF1B缺陷阻碍了LGG细胞的增殖、周期和转移，并诱导细胞死亡，可能是通过与TLK1的相互作用实现的。ASF1B和TLK1之间的相互作用促进了LGG的恶性进展。要点TLK1与ASF1B相互作用。干扰ASF1B抑制了LGG细胞的增殖、侵袭和迁移能力，并诱导了细胞周期阻滞，同时引起了凋亡。ASF1B和TLK1之间的相互作用促进了LGG的恶性进展。

Low-grade glioma (LGG), which is the second most frequent adult brain malignancy, severely threatens patients' health and has a high recurrence rate. Histone H3/H4 chaperone anti-silencing function 1 B (ASF1B) has a tight association with the initiation and development of tumours. The expression and regulation mechanism of ASF1B in LGG were discussed.ASF1B expression in LGG patients as well as the association of ASF1B with overall survival and disease-free survival of LGG patients were predicted by GEPIA database. The independent prognostic value of ASF1B in LGG patients was investigated by TCGA database. RT-qPCR, together with western blot was applied for the assessment of ASF1B in LGG cell lines. After ASF1B expression was inhibited, CCK8 and colony formation assays judged cell proliferation. Flow cytometry analysis and TUNEL assay appraised cell cycle as well as apoptosis. Cell migratory and invasive capacities were measured by wound healing as well as Transwell assays. Western blot tested the expression of proliferation-, cycle-, apoptosis-, and metastasis-associated proteins. STRING and GeneMANIA database predicted the relationship between ASF1B and tousled-like kinase 1 (TLK1). ChIP assay testified the affinity of ASF1B with TLK1. Subsequently, TLK1 was overexpressed and ASF1B expression interfered, and the functional assays were executed.ASF1B was discovered to be increased in LGG tissues and cells and indicates an unfavourable prognosis for LGG patients. ASF1B was not an independent prognostic factor for LGG. ASF1B deficiency obstructed the proliferation, cell cycle as well as metastasis of LGG cells, and induced cell death, which might be realized through the interaction with TLK1.The interaction between ASF1B and TLK1 promoted the malignant progression of LGG.Key messagesTLK1 interacts with ASF1B.Interference with ASF1B inhibits the proliferative, invasive and migratory capabilities and induces the cycle arrest, along with the apoptosis of LGG cells.The interaction between ASF1B and TLK1 promotes the malignant progression of LGG.