SMYD3在骨肉瘤U2OS细胞增殖和转移中的作用及其机制

目的:探究组蛋白甲基化酶SMYD3对骨肉瘤U2OS细胞增殖和侵袭的作用及其具体机制。方法:通过使用CRISPR-Cas9技术沉默U2OS细胞中的SMYD3基因；通过CCK-8技术检测SMYD3对于U2OS细胞增殖的影响；通过细胞Transwell实验观察SMYD3对骨肉瘤细胞迁移和侵袭的影响；通过Western Blot实验检测EMT相关蛋白（E-cadherin、N-cadherin和Vimentin）的蛋白水平变化。结果:SMYD3的表达下调可以抑制骨肉瘤U2OS细胞的增殖、迁移和侵袭能力；同时Western Blot检测发现在骨肉瘤U2OS细胞中敲除SMYD3后E-cadherin的蛋白表达量上升，而N-cadherin和Vimentin的蛋白表达量下降。结论:SMYD3与骨肉瘤的发生、转移密切相关，有可能成为骨肉瘤潜在的生物标志物和治疗靶点。

The effect and mechanism of SMYD3 in proliferation and migration of osteosarcoma U2OS cells

Objective:To investigate the effect of SMYD3 on the proliferation and invasion in osteosarcoma and corresponding underlying mechanism.Methods:SMYD3 was knocked down in U2OS through CRISPR-Cas9 technology.CCK-8 assay was used to detect the effect of SMYD3 on the proliferation of U2OS.The effect of SMYD3 on the migration and invasion of osteosarcoma cells was observed through Transwell assay.Western Blot assay was performed to detect changes of the EMT-related proteins(E-cadherin,N-cadherin and Vimentin).Results:Downregulation of SMYD3 inhibited the proliferation,migration and invasion of osteosarcoma cells.The protein expression level of E-cadherin was upregulated and N-cadherin and Vimentin were downregulated corresponding to the downregulation of SMYD3.Conclusion:SMYD3 may be closely related to the development and metastasis of osteosarcoma and be a potential biomarker and therapeutic target for osteosarcoma.