引用

神经节苷在人脑胶质瘤组织中的表达已经有一些研究。然而，这些神经节苷素如GD3和GD2的作用还没有得到很好的理解。在本研究中，我们利用基因工程的胶质瘤小鼠模型来阐明GD3在胶质瘤中的功能。在培养的p53缺陷小鼠星形胶质细胞中强制表达血小板衍生生长因子B (PDGFB)可导致GD3和GD2的表达。gd3阳性星形胶质细胞表现出细胞生长和侵袭活性增加，Akt和Yes激酶磷酸化水平升高。通过酶介导的自由基源激活(EMARS)反应和质谱分析，我们确定PDGF受体α (PDGFR α)为gd3相关分子。gd3阳性星形胶质细胞显示大量PDGFR α;与gd3阴性细胞相比，富含糖脂的微畴(GEM)/筏。Src激酶家族Yes与PDGFR alpha;共同沉淀，其在gd3阳性星形胶质细胞细胞侵袭增加中的关键作用通过抗Yes siRNA沉默得到证实。PDGFR之间的直接联系; and GD3 was also shown, suggesting that GD3 forms a ternary complex with PDGFR alpha; and Yes. The fact that GD3, PDGFR alpha; and activated Yes were colocalized in lamellipodia and edge of tumors in cultured cells and glioma tissues, respectively, suggest that GD3 induced by PDGFB enhances PDGF signals in GEM/rafts, leading to the promotion of malignant phenotypes such as cell invasion in gliomas. Copyright 2015, The American Society for Biochemistry and Molecular Biology.