Despite intensive research, brain tumors remain among the most difficult type of malignancies to treat, due largely to their diffusely invasive nature and the associated difficulty of adequate surgical resection. To migrate through the brain parenchyma and to proliferate, glioma cells must be capable of significant changes in shape and volume. We have previously reported that glioma cells express an amiloride- and psalmotoxin-sensitive cation conductance that is not found in normal human astrocytes. In the present study, we investigated the potential role of this ion channel to mediate regulatory volume increase in glioma cells. We found that the ability of the cells to volume regulate subsequent to cell shrinkage by hyperosmolar solutions was abolished by both amiloride and psalmotoxin 1. This toxin is thought to be a specific peptide inhibitor of acid-sensing ion channel (ASIC1), a member of the Deg/ENaC superfamily of cation channels. We have previously shown this toxin to be an effective blocker of the glioma cation conductance. Our data suggest that one potential role for this conductance may be to restore cell volume during the cell's progression thorough the cell cycle and while the tumor cell migrates within the interstices of the brain.

译文

尽管进行了深入的研究,但脑肿瘤仍然是最难治疗的恶性肿瘤之一,这主要是由于其弥漫性侵袭性和相关的手术切除困难。为了通过脑实质迁移并增殖,神经胶质瘤细胞必须能够在形状和体积上发生重大变化。我们以前曾报道过,神经胶质瘤细胞表达对阿米洛利和海参毒素敏感的阳离子电导,这在正常人星形胶质细胞中找不到。在本研究中,我们研究了该离子通道在介导神经胶质瘤细胞中调节体积增加的潜在作用。我们发现,阿米洛利和psalmotoxin 1都消除了高渗溶液引起细胞收缩后细胞体积调节的能力。该毒素被认为是酸感应离子通道 (ASIC1) 的特定肽抑制剂,后者是Deg/ENaC阳离子通道超家族的成员。我们以前已经证明这种毒素是神经胶质瘤阳离子电导的有效阻滞剂。我们的数据表明,这种电导的一个潜在作用可能是在细胞整个细胞周期的进展过程中以及肿瘤细胞在大脑间隙内迁移时恢复细胞体积。

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