METHODS: Cell proliferation, invasion, apoptosis, and cell cycle of meningiomas were determined by cell counting kit-8 assay, transwell assay, and flow cytometry, respectively. The expression of SAC in meningioma cells was detected by quantitative real-time polymerase chain reaction and Western blot. The interaction between anaphase promoting complex/cyclosome (APC/C) and cell division cycle 20 (Cdc20) protein in meningioma cells was further explored by co-immunoprecipitation.
RESULTS: We found that the expression of NF2/merlin was low or absent in malignant meningiomas. Overexpression of NF2 suppressed the proliferation and invasion of meningioma cells, prolonged the G2/M phase, and elevated the expression of SAC proteins at posttranscription. Furthermore, the interaction between APC/C and Cdc20 was inhibited by NF2.
CONCLUSIONS: Our findings suggested that NF2 might restore SAC function by impairing the binding of APC/C and Cdc20, thereby limiting the mitotic rate and inhibiting proliferation of meningiomas.
方法:细胞增殖,入侵,凋亡,通过细胞计数试剂盒-8测定脑膜瘤的细胞周期,transwell分析,和流式细胞术,分别。通过实时定量聚合酶链反应和Westernblot检测脑膜瘤细胞中SAC的表达。通过免疫共沉淀进一步研究了脑膜瘤细胞中后期促进复合物/环小体(APC/C)与细胞分裂周期20(Cdc20)蛋白之间的相互作用。
结果:我们发现NF2/merlin在恶性脑膜瘤中的表达较低或不存在。NF2过表达抑制脑膜瘤细胞的增殖和侵袭,延长G2/M阶段,并在转录后提高SAC蛋白的表达。此外,NF2抑制了APC/C与Cdc20的相互作用。
结论:我们的研究结果表明,NF2可能通过削弱APC/C和Cdc20的结合来恢复SAC功能,从而限制有丝分裂率并抑制脑膜瘤的增殖。