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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. TLK1 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.

The interaction between ASF1B and TLK1 promotes the malignant progression of low-grade glioma