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一种裂解的脑特异性细胞外基质蛋白的表达介导胶质瘤细胞在体内的侵袭。

Expression of a cleaved brain-specific extracellular matrix protein mediates glioma cell invasion In vivo.

作者信息

Zhang H, Kelly G, Zerillo C, Jaworski D M, Hockfield S

机构信息

Section of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06520-8001, USA.

出版信息

J Neurosci. 1998 Apr 1;18(7):2370-6. doi: 10.1523/JNEUROSCI.18-07-02370.1998.

Abstract

Malignant gliomas (primary brain tumors) aggressively invade the surrounding normal brain. This invasive ability is not demonstrated by brain metastases of nonglial cancers. The brain-specific, brain-enriched hyaluronan binding (BEHAB)/brevican gene, which encodes an extracellular hyaluronan-binding protein, is consistently expressed by human glioma and is not expressed by tumors of nonglial origin (Jaworski et al., 1996). BEHAB/brevican can be cleaved into an N-terminal fragment that contains a hyaluronan-binding domain (HABD) and a C-terminal fragment (Yamada et al., 1995). Here, using antisera to peptides in the predicted N-terminal and C-terminal proteolytic fragments, we demonstrate that the BEHAB/brevican protein is cleaved in invasive human and rodent gliomas. A role for this protein in glioma cell invasion was tested by transfecting a noninvasive cell line with the BEHAB/brevican gene. The noninvasive 9L glioma cell was transfected with either full-length BEHAB/brevican or the HABD and tested for invasion in in vitro and in vivo invasion assays. Although both constructs increased invasion in vitro, only the HABD increased invasion by tumors growing in vivo. Experimental intracranial tumors from full-length transfectants showed no increase in invasion over control tumors, whereas tumors from HABD transfectants showed a marked potentiation of tumor invasion, producing new tumor foci at sites distant from the main tumor mass. This work demonstrates a role for a brain-specific extracellular matrix protein in glioma invasion, opening new therapeutic avenues for a uniformly fatal disease.

摘要

恶性胶质瘤(原发性脑肿瘤)会侵袭周围正常脑组织。非神经胶质癌的脑转移瘤则不具备这种侵袭能力。脑特异性、脑富集透明质酸结合蛋白(BEHAB)/短蛋白聚糖基因编码一种细胞外透明质酸结合蛋白,在人类胶质瘤中持续表达,而在非神经胶质起源的肿瘤中不表达(Jaworski等人,1996年)。BEHAB/短蛋白聚糖可被切割成一个包含透明质酸结合域(HABD)的N端片段和一个C端片段(Yamada等人,1995年)。在此,我们使用针对预测的N端和C端蛋白水解片段中肽段的抗血清,证明BEHAB/短蛋白聚糖蛋白在侵袭性人类和啮齿动物胶质瘤中被切割。通过用BEHAB/短蛋白聚糖基因转染非侵袭性细胞系,测试了该蛋白在胶质瘤细胞侵袭中的作用。将非侵袭性9L胶质瘤细胞用全长BEHAB/短蛋白聚糖或HABD转染,并在体外和体内侵袭试验中测试其侵袭能力。虽然两种构建体都增加了体外侵袭,但只有HABD增加了体内生长肿瘤的侵袭能力。全长转染体的实验性颅内肿瘤与对照肿瘤相比侵袭性没有增加,而HABD转染体的肿瘤显示出肿瘤侵袭的显著增强,在远离主要肿瘤块的部位产生新的肿瘤病灶。这项工作证明了一种脑特异性细胞外基质蛋白在胶质瘤侵袭中的作用,为这种一致致命的疾病开辟了新的治疗途径。

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