神经黏附分子NECL1抑制神经胶质瘤细胞的迁移、侵袭并诱导其分化

目的 在NECL1表达缺失的神经胶质瘤细胞系中探讨神经黏附分子NECL1恢复表达后对肿瘤细胞迁移及侵袭的影响.方法 在U251胶质瘤细胞系中,通过划痕及Transwell实验观察NECL1恢复表达后对肿瘤细胞迁移及侵袭的影响,通过对细胞外金属蛋白酶活性的检测证明NECL1恢复表达后对肿瘤侵袭能力的影响.利用不同培养密度的U251细胞,对NECL1恢复表达后细胞形态进行观察,并通过Western blot实验验证相关蛋白的表达.结果 在NECL1表达缺失的胶质瘤细胞系U251中,恢复NECL1的表达后,肿瘤细胞的迁移及侵袭受到了抑制. NECL1恢复表达的U251细胞有向星形胶质细胞分化的趋势,星形胶质细胞标志蛋白神经胶质纤维酸性蛋白的表达上调.结论 神经黏附分子NECL1作为一个潜在的胶质瘤抑制因子,对肿瘤细胞的迁移和侵袭能力均有不同程度抑制作用,同时,NECL1具有诱导神经胶质瘤U251细胞向星形胶质细胞方向分化的潜能.

Neural Adhesion Molecule NECL1 Inhibits Migration, Invasion,and Potentially Induces Differentation of Glioma Cell

Objective To explore the influences of the restoration of neural adhesion molecule NECL1 on the morphology, migration, and invasion of NECL1-deficient glioma cell lines. MethodsScratch and Transwell assays were used to observe the cell migration and invasion, the activities of extracellular metalloproteinases were measured, and the cell morphology was observed. Astrocytes marker glial fibrillary acidic protein was detected by Western blot after the restoration of NECL1 in glioma U251 cell line. ResultsIn NECL1-deficient U251 glioma cell lines, migration and invasion were inhibited. The U251 cells was differentiated potentially to astrocytes, and glial fibrillary acidic protein was up-regulated after the restoration of the NECL1 expression. ConclusionAs a potential tumor repressor, the neural adhesion molecule NECL1 can inhibitthe migration and invasion of glioma cell and induces its differentation.