Induction of oligodendrogenesis in glioblastoma-initiating cells by IFN-mediated activation of STAT3 signaling
Induction of oligodendrogenesis in glioblastoma-initiating cells by IFN-mediated activation of STAT3 signaling
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DOI：
10.1016/j.canlet.2009.04.020
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发表时间：
2009-10-18
期刊：
影响因子：
9.7
通讯作者：
Wakabayashi, Toshihiko
中科院分区：
文献类型：
--
作者：
Yuki, Kanako;Natsume, Atsushi;Wakabayashi, Toshihiko
癌症患者对干扰素（IFN）治疗的反应是持久的，表明IFN可能作用于小的癌症干细胞群体。胶质瘤起始细胞（GIC）可以自我更新并诱导形成异质分化的肿瘤细胞，并且对替莫唑胺等化疗药物具有抗性。在这项研究中，我们发现，通过STAT 3信号，IFN-β抑制GIC的增殖，自我更新和肿瘤发生，诱导其终末分化为成熟的少突胶质细胞样细胞，并表现出协同细胞毒性与替莫唑胺。因此，IFN可能是诱导GIC终末分化的潜在治疗剂。(C)2009爱思唯尔爱尔兰有限公司保留所有权利。
The response of cancer patients to interferon (IFN) treatment is long-lasting, indicating that IFN may act on small cancer stem cell populations. Glioma-initiating cells (GICs) can self-renew and induce the formation of heterogeneously differentiated tumor cells and are resistant to chemotherapeutic agents like temozolomide. In this study, we showed that via STAT3 signaling, IFN-beta suppressed the proliferation, self-renewal, and tumorigenesis of GICs, induced their terminal differentiation to mature oligodendroglia-like cells, and exhibited synergistic cytotoxicity with temozolomide. Therefore, IFN may be a potential therapeutic agent for inducing the terminal differentiation of GICs. (C) 2009 Elsevier Ireland Ltd. All rights reserved.