靶向沉默髓鞘转录因子MyT1对脑胶质瘤细胞恶性生物学行为的影响

目的 探讨靶向沉默髓鞘转录因子1（MyT1）对人脑胶质瘤细胞迁移、侵袭和黏附的影响和相关分子机制。方法 设计特异性靶向沉默MyT1基因的shRNA，包装慢病毒后感染人脑胶质瘤U-118MG和U-87MG细胞，qPCR和Western blot检测两种细胞中MyT1的表达水平，BrdU实验、细胞划痕实验、Transwell实验和细胞黏附实验分别检测两种细胞的迁移、侵袭和黏附能力的变化，qPCR检测细胞黏附和肿瘤转移相关基因的表达水平。结果 在HEK293T细胞中包装了特异性靶向MyT1基因的shRNA慢病毒，并成功感染了U-118MG和U-87MG细胞；两种细胞中MyT1 mRNA和蛋白表达水平均显著下调（均P<0.05），细胞的迁移、侵袭和黏附能力均有一定程度的降低（均P<0.05），细胞黏附相关基因表达水平显著下降，肿瘤转移相关基因表达水平显著上升（均P<0.05）。结论 靶向沉默MyT1基因对人脑胶质瘤U-118MG和U-87MG细胞的迁移、侵袭和黏附能力有抑制作用，其机制可能与调控细胞黏附和肿瘤转移相关基因的表达有关。MyT1基因的表达，可能是脑胶质瘤诊疗的一个潜在靶标。

Effect of Targeted Knockdown of MyT1 Gene on Malignant Biological Behavior of Glioblastoma Cells

Objective To investigate the effects and molecular mechanisms of targeted knockdown of MyT1 on the migration, invasion and adhesion of human glioblastoma cells. Methods shRNA specifically targeting MyT1 gene was designed, and the packaged lentivirus was used to infect human glioblastoma U-118MG and U-87MG cells. The expression levels of MyT1 mRNA and protein in U-118MG and U-87MG cells were detected by qPCR and Western blot. The migration, invasion and adhesion of U-118MG and U-87MG cells were respectively detected by BrdU assay, cell would healing assay, Transwell assay and adhesion assay. The expression levels of genes related to cell adhesion and tumor metastasis were detected by qPCR. Results The lentivirus specifically targeting MyT1 gene was successfully packaged in HEK293T cells and then infected U-118MG and U-87MG cells. The expression levels of MyT1 mRNA and protein were significantly downregulated (both P<0.05), and the migration, invasion and adhesion abilities of cells were decreased (all P<0.05). The expression level of cell adhesion-related genes decreased significantly, while the expression level of tumor metastasis-related genes increased significantly (both P<0.05). Conclusion Targeted knockdown of MyT1 gene inhibits the migration, invasion and adhesion of human glioblastoma U-118MG and U-87MG cells, and the mechanism may be related to the regulation of cell adhesion- and tumor metastasis-related genes expression. MyT1 may be a potential target for the diagnosis and treatment of glioblastoma.