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首页> 外文期刊>Expert opinion on therapeutic targets >Temozolomide induces the expression of the glioma Big Potassium (gBK) ion channel, while inhibiting fascin-1 expression: possible targets for glioma therapy
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Temozolomide induces the expression of the glioma Big Potassium (gBK) ion channel, while inhibiting fascin-1 expression: possible targets for glioma therapy

机译：替莫唑胺诱导神经胶质瘤大钾（gBK）离子通道的表达，同时抑制fascin-1表达：神经胶质瘤治疗的可能靶点

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摘要

Objective: Temozolomide (TMZ) improves Glioblastoma Multiforme (GBM) patient survival. The invasive behavior of the glioma cells is the cause of GBM relapse. The glioma BK ion channel (gBK) may provide glioma cells with a mechanism to invade surrounding tissue. gBK contains epitopes that cytolytic T lymphocytes (CTLs) can recognize and kill glioma cells. Fascin-1 is an actin crosslinking molecule that supports microvilli; these membrane protrusions provide a physical defense against CTLs. TMZ was investigated to determine its effect on gBK and fascin-1 expression.Research design and methods: Human glioma cells cultured in TMZ were analyzed for their altered mRNA and gBK protein levels by using quantitative real time PCR, immunostaining and cellular functional assays.Results: TMZ slowed glioma cell growth and inhibited their transmigratory properties due to loss of fascin-1. TMZ induced increased gBK and HLA expression and allowed these TMZ-treated cells to become better targets for gBK-specific CTLs.Conclusions: Besides its traditional chemotherapeutic effect, TMZ can have four other targeted pathways: 1) slowed glioma cell growth; 2) inhibited glioma cell transmigration; 3) increased HLA-A2 and gBK tumor antigen production; 4) increased CTL-mediated cytolysis of the TMZ treated glioma cells due to the loss of their defensive membrane protrusions supported by fascin-1.
机译：目的：替莫唑胺（TMZ）提高多形性胶质母细胞瘤（GBM）患者的生存率。胶质瘤细胞的侵袭行为是GBM复发的原因。胶质瘤BK离子通道（gBK）可以为胶质瘤细胞提供侵袭周围组织的机制。 gBK包含表位，细胞溶解性T淋巴细胞（CTL）可以识别并杀死神经胶质瘤细胞。 Fascin-1是肌动蛋白交联分子，支持微绒毛。这些膜突出物可抵御CTL。研究设计和方法：通过实时定量PCR，免疫染色和细胞功能分析法分析TMZ中培养的人神经胶质瘤细胞的mRNA和gBK蛋白水平的变化。 ：TMZ减慢了fascin-1的丧失，从而减缓了神经胶质瘤细胞的生长并抑制了其迁移特性。 TMZ诱导增加的gBK和HLA表达，并使这些经TMZ处理的细胞成为针对gBK特异性CTL的更好靶标。 2）抑制神经胶质瘤细胞的迁移; 3）增加HLA-A2和gBK肿瘤抗原产生; 4）由于由fascin-1支持的防御膜突起的丧失，TMZ处理的神经胶质瘤细胞的CTL介导的细胞溶解增加。

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