GLIOBLASTOMA EXPRESSION OF VITRONECTIN AND THE ALPHA-V-BETA-3 INTEGRIN - ADHESION MECHANISM FOR TRANSFORMED GLIAL-CELLS
GLIOBLASTOMA EXPRESSION OF VITRONECTIN AND THE ALPHA-V-BETA-3 INTEGRIN - ADHESION MECHANISM FOR TRANSFORMED GLIAL-CELLS
复制标题
DOI：
10.1172/jci115516
复制
发表时间：
1991-12-01
影响因子：
15.9
通讯作者：
CHERESH, DA
中科院分区：
文献类型：
--
作者：
GLADSON, CL;CHERESH, DA
多形性胶质母细胞瘤是最恶性的星形胶质细胞源性肿瘤，生长为粘附性肿块并局部侵入正常脑。对成人脑胶质母细胞瘤活检材料进行的可能增强粘附和侵袭的粘附蛋白表达的检查证实了肿瘤细胞相关的玻连蛋白（5/5）。相反，在低级别星形胶质细胞肿瘤（0/4）、反应性星形胶质细胞增生（0/4）或正常成人皮质和大脑白色物质（0/5）中未检测到玻连蛋白与胶质细胞相关。此外，胶质母细胞瘤肿瘤实质中不存在多种其他粘附配体。α-v-β-3整联蛋白是胶质母细胞瘤原位鉴定的唯一玻连蛋白受体，并且在低级别星形胶质细胞衍生的肿瘤、反应性星形胶质细胞增生或正常成人皮质和大脑白色物质中的胶质细胞或神经元上也不表达。在细胞附着试验中，培养的胶质母细胞瘤细胞附着到胶质母细胞瘤肿瘤冷冻切片的实质中的玻连蛋白表达位点，但未能附着到正常脑。这种粘附被针对玻连蛋白、α-v-β-3整联蛋白的抗体和含有Arg-Gly-Asp的肽抑制。这些数据为胶质母细胞瘤肿瘤中的细胞粘附机制提供了证据，该机制可能增强胶质母细胞瘤细胞对正常脑的侵袭。
Glioblastoma multiforme, the most malignant astroglial-derived tumor, grows as an adherent mass and locally invades normal brain. An examination of adult cerebral glioblastoma biopsy material for the expression of adhesive proteins that might potentiate adhesion and invasion demonstrated tumor cell-associated vitronectin (5/5). In contrast, vitronectin was not detected associated with glial cells in low grade astroglial tumors (0/4), reactive astrogliosis (0/4), or in normal adult cortex and cerebral white matter (0/5). Also, a wide variety of other adhesive ligands were absent from the glioblastoma tumor parenchyma. The alpha-v-beta-3 integrin was the only vitronectin receptor identified in glioblastoma tumors in situ, and was also not expressed on low grade astroglial-derived tumors, reactive astrogliosis, or on glia or neurons in normal adult cortex and cerebral white matter. In a cell attachment assay, cultured glioblastoma cells attached to the parenchyma of glioblastoma tumor cryostat sections at the sites of vitronectin expression, but failed to attach to normal brain. This adhesion was inhibited by antibodies directed against vitronectin, the alpha-v-beta-3 integrin, and with an Arg-Gly-Asp-containing peptide. These data provide evidence for a cell adhesion mechanism in glioblastoma tumors that might potentiate glioblastoma cell invasion of normal brain.