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首页> 外文期刊>Archives of medical research >gamma-secretase inhibitor-I enhances radiosensitivity of glioblastoma cell lines by depleting CD133+ tumor cells.
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gamma-secretase inhibitor-I enhances radiosensitivity of glioblastoma cell lines by depleting CD133+ tumor cells.

机译：γ-分泌酶抑制剂-I通过消耗CD133 +肿瘤细胞来增强胶质母细胞瘤细胞系的放射敏感性。

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BACKGROUND AND AIMS: Glioblastoma is a deadly primary brain tumor with great resistance to radiotherapy. To reverse its radioresistance is important for improving prognosis. Gamma-secretase inhibitors (GSI) have been proven to have anti-tumor effects, yet the knowledge of their influences on glioblastomas is still limited. METHODS: The cytotoxic effects of GSI-I (a tripeptide GSI) on glioblastoma cell lines U87 and U251 were assessed by MTT assay, and the low concentration that did not induce significant cell death was determined. The in vitro radiosensitization effects of this low concentration of GSI-I were evaluated by cell colony forming assays. The CD133+ cell fractions before and after radiation with or without treatment of GSI-I were analyzed by flow cytometry. Then CD133+ and CD133- glioblastoma cells were sorted by magnetic activated cell sorting (MACS), and the radiosensitization effects of GSI-I on the two cell subtypes were investigated separately. Finally, the cytotoxic effects of GSI-I on CD133+and CD133- glioblastoma cells were examined, respectively, and the expression of the Notch pathway components between the two cell subtypes were compared. In addition, the anti-tumor effects of GSI-I were confirmed by in vivo experiments. RESULTS: GSI-I at a low concentration sensitized U87 and U251 cells to radiation by depletion of radioresistant CD133+ cells. CD133+ U87/U251 cells displayed preferential sensitivity to low concentrations of GSI-I, which may be related to the higher expression of the Notch signaling pathway in these cells. CONCLUSIONS: Combining GSI-I with radiotherapy may represent a promising strategy for treating radioresistant gliomas.
机译：背景与目的：胶质母细胞瘤是一种致命的原发性脑肿瘤，对放疗有很大的抵抗力。逆转其放射抵抗对改善预后很重要。 γ-分泌酶抑制剂（GSI）已被证明具有抗肿瘤作用，但其对胶质母细胞瘤影响的知识仍然有限。方法：采用MTT法评估了GSI-1（三肽GSI）对胶质母细胞瘤细胞U87和U251的细胞毒性作用，并确定了未诱导细胞死亡的低浓度。通过细胞集落形成测定法评估了这种低浓度的GSI-1的体外放射增敏作用。通过流式细胞术分析在用或不用GSI-1处理的辐射前后的CD133 +细胞级分。然后通过磁活化细胞分选术（MACS）分选CD133 +和CD133-胶质母细胞瘤细胞，并分别研究GSI-1对这两种细胞亚型的放射增敏作用。最后，分别检查了GSI-1对CD133 +和CD133-胶质母细胞瘤细胞的细胞毒性作用，并比较了两种亚型之间Notch途径成分的表达。另外，通过体内实验证实了GSI-1的抗肿瘤作用。结果：低浓度的GSI-1通过耗尽抗辐射的CD133 +细胞使U87和U251细胞对辐射敏感。 CD133 + U87 / U251细胞显示出对低浓度GSI-1的优先敏感性，这可能与这些细胞中Notch信号通路的更高表达有关。结论：将GSI-1与放射疗法相结合可能代表了一种治疗放射线胶质瘤的有前途的策略。

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