Koochekpour S, Pilkington G J, Merzak A
Department of Neuropathology, Institute of Psychiatry, London, UK.
Int J Cancer. 1995 Nov 3;63(3):450-4. doi: 10.1002/ijc.2910630325.
The mechanisms underlying the invasive properties of gliomas, the major form of intrinsic brain tumours in humans, are poorly understood. We have reported that CD44 plays an important role in this behaviour in vitro. In the present work, we investigated the role of its ligand, hyaluronic acid (HA), in invasion in 8 human glioma cell lines. We found that HA mediates cell detachment via its interaction with its high affinity receptor, CD44H. Using 8 microns porosity polycarbonate filter transwells, we demonstrate that HA strongly stimulates migration in all 8 cell lines. This effect was found to be partially counteracted by a CD44H monoclonal antibody (MAb), suggesting the involvement of CD44H, as well as other HA receptors, in this process. Furthermore, incorporation of increasing concentrations of HA in Matrigel in an in vitro invasion assay resulted in a substantial increase in the invasive propensity of the glioma cell lines. Moreover, blocking experiments with the CD44H MAb suggest that CD44H and other receptors interact with HA to promote cell invasion in vitro. Our results show that HA induces cell detachment, stimulates migration and promotes invasion via its interaction with CD44H and other HA receptors in vitro. These effects could be prevented by use of specific HA receptor antibodies.
胶质瘤是人类颅内原发性肿瘤的主要形式,其侵袭特性的潜在机制目前仍知之甚少。我们曾报道,CD44在体外的这种行为中起重要作用。在本研究中,我们调查了其配体透明质酸(HA)在8种人类胶质瘤细胞系侵袭过程中的作用。我们发现,HA通过与高亲和力受体CD44H相互作用介导细胞脱离。使用孔径为8微米的聚碳酸酯滤膜Transwell小室,我们证明HA能强烈刺激所有8种细胞系的迁移。发现这种效应部分被CD44H单克隆抗体(MAb)抵消,这表明CD44H以及其他HA受体参与了这一过程。此外,在体外侵袭实验中,向基质胶中加入浓度递增的HA会导致胶质瘤细胞系的侵袭倾向显著增加。而且,用CD44H MAb进行的阻断实验表明,CD44H和其他受体与HA相互作用以促进体外细胞侵袭。我们的结果表明,HA在体外通过与CD44H和其他HA受体相互作用诱导细胞脱离、刺激迁移并促进侵袭。使用特异性HA受体抗体可防止这些效应。