类风湿性关节炎（RA）是一种常见的疾病，伴有关节软骨破坏。BUB1有丝分裂检查点丝氨酸/苏氨酸激酶（BUB1）在RA患者滑膜组织中异常表达，但其对RA的影响尚不清楚。本研究旨在探讨BUB1在RA中的作用。通过用肿瘤坏死因子-α（TNF-α）处理MH7A细胞构建RA细胞模型，利用Western印迹检测了MH7A细胞中BUB1、GAPDH、磷酸化磷脂三醇3激酶（p-PI3K）/PI3K、磷酸化丝氨酸/苏氨酸激酶（p-Akt）/Akt的水平。采用集落形成实验检测了MH7A细胞的增殖，利用划痕愈合实验和透过性实验检测了MH7A细胞的迁移和侵袭能力。通过定量逆转录聚合酶链反应评估了炎性细胞因子的mRNA水平。结果表明，沉默BUB1抑制了TNF-α诱导的MH7A细胞增殖、迁移和侵袭。沉默BUB1抑制了TNF-α诱导的MH7A细胞中PI3K/Akt途径。我们还发现，si-BUB1转染抑制了TNF-α诱导的MH7A细胞增殖、迁移和侵袭，而这些效果被PI3K途径的激活剂740Y-P的共同处理所减弱。沉默BUB1减少了炎性细胞因子的表达。通过PI3K/Akt途径，沉默BUB1抑制了TNF-α诱导的MH7A细胞增殖、迁移和侵袭。© 2023亚太风湿病协会联盟和John Wiley & Sons Australia，有限公司。

Rheumatoid arthritis (RA) is a common disease with joint cartilage destruction. BUB1 Mitotic Checkpoint Serine/Threonine Kinase (BUB1) is abnormally expressed in synovial tissues of RA patients, but its effect on RA remains unclear. In this study, we explored the role of BUB1 in RA.An RA cell model was constructed by treating MH7A cells with tumor necrosis factor-α (TNF-α). The levels of BUB1, GAPDH, phosphorylated phosphatidylinositol 3 kinase (p-PI3K)/PI3K, and phosphorylated serine/threonine kinase (p-Akt)/Akt in MH7A cells were examined by Western blot. The MH7A cell proliferation was examined by colony formation assay. Wound healing assay and transwell assay were carried out to detect MH7A cell migration and invasion. The mRNA levels of proinflammatory cytokines were assessed by quantitative reverse transcription polymerase chain reaction.The results showed that knockdown BUB1 inhibited TNF-α-induced MH7A cell proliferation, migration, and invasion. Silencing BUB1 repressed the PI3K/Akt pathway in TNF-α-induced MH7A cells. We also found that the TNF-α-induced MH7A cell proliferation, migration, and invasion were repressed by si-BUB1 transfection, whereas these effects were attenuated by 740Y-P (an activator of the PI3K pathway) co-treatment. Knockdown of BUB1 reduced the expression of the proinflammatory cytokines.Knockdown BUB1 repressed TNF-α-induced MH7A cell proliferation, migration and invasion through the PI3K/Akt pathway.© 2023 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons Australia, Ltd.