NCAPG2 (non-SMC condensin II complex subunit G2), as an important factor in cell mitosis, has been the focus in the study of different cancers. However, the role of NCAPG2 in the malignancy of glioblastoma cells remains unknown. The findings from the present study demonstrated that NCAPG2 was significantly increased in human glioblastoma tissues and was associated with poor clinical outcome. Moreover, NCAPG2 could promote proliferation, migration, and invasion and regulate cell cycle in glioblastoma cells. Investigation of the molecular mechanism indicated that NCAPG2 regulated HBO1 phosphorylation and H4 histone acetylase activation, modulated the activation of Wnt/β-catenin pathway, and the binding of MCM protein to chromatin to exert its role. Furthermore, knockdown of HBO1 was found to reverse the effect of NCAPG2 overexpression on cell proliferation, migration, invasion, and cell cycle. In addition, knockdown of NCAPG2 attenuated glioblastoma tumorigenesis in vivo. Taken together, the findings demonstrated that NCAPG2 facilitates the malignancy of glioblastoma cells and xenograft tumor growth via HBO1 activation by phosphorylation. These results improve our understanding of the mechanism underlying glioblastoma progression and may contribute to the identification of novel biomarkers and therapeutic targets for glioblastoma.

中文翻译：

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NCAPG2 通过磷酸化 HBO1 激活促进胶质母细胞瘤细胞的恶性肿瘤和异种移植肿瘤生长


NCAPG2（非SMC凝缩蛋白II复合物亚基G2）作为细胞有丝分裂的重要因子，一直是不同癌症研究的焦点。然而，NCAPG2 在胶质母细胞瘤细胞恶性肿瘤中的作用仍不清楚。本研究的结果表明，NCAPG2 在人胶质母细胞瘤组织中显着增加，并且与不良的临床结果相关。此外，NCAPG2可以促进胶质母细胞瘤细胞的增殖、迁移和侵袭并调节细胞周期。分子机制研究表明，NCAPG2通过调节HBO1磷酸化和H4组蛋白乙酰化酶激活，调节Wnt/β-catenin通路的激活，以及MCM蛋白与染色质的结合来发挥其作用。此外，发现 HBO1 的敲低可以逆转 NCAPG2 过表达对细胞增殖、迁移、侵袭和细胞周期的影响。此外，NCAPG2 的敲低可减弱体内胶质母细胞瘤的肿瘤发生。综上所述，研究结果表明，NCAPG2 通过磷酸化激活 HBO1，促进胶质母细胞瘤细胞的恶性和异种移植肿瘤的生长。这些结果提高了我们对胶质母细胞瘤进展机制的理解，并可能有助于识别胶质母细胞瘤的新型生物标志物和治疗靶点。