Huang Jiang-mei, Tian Xin-xia, Zhong Yan-feng, Ma De-lian, Ma Yue, You Jiang-feng, Zhang Yan
Department of Pathology, Health Science Center, Peking University, Beijing 100083, China.
Zhonghua Bing Li Xue Za Zhi. 2006 Aug;35(8):478-82.
To investigate the effects of beta1-integrin, fibronectin (FN) and laminin (LN) on the invasive behavior of human gliomas.
Functional impacts of beta1-integrin, fibronectin and laminin on cell adhesion, migration and metastasis of U251 malignant glioblastoma cells were investigated by in vitro adhesion, migration and invasion assays. The amount and distributions of cellular microfilaments and pseudopodia were studied by fluorescent cytochemistry, confocal laser scanning microscope and scanning electron microscope. Lastly, beta1-integrin, fibronectin and laminin were investigated for their roles in cellular microfilament skeleton.
(1) Fibronectin did not affect cell adhesion of U251MG cells, but anti-beta1 integrin antibodies inhibited cell adhesion (P < 0.01); Laminin stimulated cell adhesion of U251MG cells (P < 0.01) but anti-beta1 integrin antibodies had little effect on the laminin-mediated cell adhesion. (2) The migration of U251MG cells on dishes coated with FN was inhibited by anti-beta1 integrin antibodies (P < 0.05). (3) F-actins formed strong and dense stress fibers in U251MG cells on dishes coated with FN and LN. Anti-beta1 integrin antibodies disrupted the microfilament network and F-actin aggregation. (4) FN and LN increased the number of pseudopodia on cell surface, whereas anti-beta1 integrin antibodies reversed this function. (5) FN and anti-beta1 integrin antibodies had little effects on the invasive ability of U251MG cells in vitro. The invasion was increased by LN, but inhibited by anti-beta1 integrin antibodies.
(1) The interaction between beta1-integrin, FN may stimulate U251MG cell migration via changing the structures of microfilament skeleton and the number of pseudopodia. (2) beta1-integrin may play a role in the LN-mediated in vitro invasion of U251MG cells.
研究β1整合素、纤连蛋白（FN）和层粘连蛋白（LN）对人胶质瘤侵袭行为的影响。
通过体外黏附、迁移和侵袭实验，研究β1整合素、纤连蛋白和层粘连蛋白对U251恶性胶质母细胞瘤细胞黏附、迁移和转移的功能影响。采用荧光细胞化学、共聚焦激光扫描显微镜和扫描电子显微镜研究细胞微丝和伪足的数量及分布。最后，研究β1整合素、纤连蛋白和层粘连蛋白在细胞微丝骨架中的作用。
（1）纤连蛋白不影响U251MG细胞的黏附，但抗β1整合素抗体抑制细胞黏附（P<0.01）；层粘连蛋白刺激U251MG细胞的黏附（P<0.01），但抗β1整合素抗体对层粘连蛋白介导的细胞黏附影响不大。（2）抗β1整合素抗体抑制U251MG细胞在涂有纤连蛋白的培养皿上的迁移（P<0.05）。（3）在涂有纤连蛋白和层粘连蛋白的培养皿上，U251MG细胞中的F-肌动蛋白形成强而密集的应力纤维。抗β1整合素抗体破坏微丝网络和F-肌动蛋白聚集。（4）纤连蛋白和层粘连蛋白增加细胞表面伪足的数量，而抗β1整合素抗体则逆转此功能。（5）纤连蛋白和抗β1整合素抗体对U251MG细胞的体外侵袭能力影响不大。层粘连蛋白增加侵袭，但抗β1整合素抗体抑制侵袭。
（1）β1整合素与纤连蛋白之间的相互作用可能通过改变微丝骨架结构和伪足数量来刺激U251MG细胞迁移。（2）β1整合素可能在层粘连蛋白介导的U251MG细胞体外侵袭中起作用。
