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Combination of lithium chloride and pEGFP-N1-BmK CT effectively decreases proliferation and migration of C6 glioma cells

机译:氯化锂和pEGFP-N1-BmK CT的组合可有效降低C6胶质瘤细胞的增殖和迁移

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Deleterious invasiveness of glioma cells into the normal brain tissue is endorsed by its inherent ability to regulate the receptor-mediated adhesive properties, extracellular matrix degradation and remodeling and elevated secretory ability of metalloproteinase (MMPs) such as MMP-2. By doing so, it will create an intercellular space for the invasion of glioma cells. Here, we reported that combination of gene therapy Buthus martensii Karsch (BmK) CT, a type of scorpion toxin peptide, with lithium chloride (LiCl), clinically used as mood stabilizer, could inhibit the migration and invasion of C6 glioma cells. The results showed that concomitant administration of LiCl and pEGFP-N1-BmK CT on glioma cells would hamper pro-MMP2 secretion and in the meantime, inhibited its proliferation in a synergistic manner. These results try to extrapolate the potential interplay between the combined treatment of LiCl and BmK CT with signaling pathways β-catenin, MMP, GSK-3 in C6 glioma cells. This strategy can stand for a novel approach designated for the development of a new method for glioma therapy.
机译:胶质瘤细胞对正常脑组织的有害侵入性受到其调节受体介导的粘附特性,细胞外基质降解和重塑以及金属蛋白酶(MMPs)如MMP-2分泌能力增强的固有能力的认可。这样,它将为胶质瘤细胞的入侵创造一个细胞间空间。在这里,我们报道基因疗法Buthus martensii Karsch(BmK)CT(一种蝎毒素肽)与氯化锂(LiCl)的组合(临床上用作情绪稳定剂)可以抑制C6胶质瘤细胞的迁移和侵袭。结果表明,在胶质瘤细胞上同时施用LiCl和pEGFP-N1-BmK CT会抑制pro-MMP2的分泌,同时以协同方式抑制其增殖。这些结果试图推断在C6神经胶质瘤细胞中,LiCl和BmK CT联合治疗与信号通路β-catenin,MMP,GSK-3之间的潜在相互作用。该策略可以代表一种新方法,该新方法被指定用于开发神经胶质瘤治疗新方法。

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