The role of STAT3 in glioblastoma progression through dual influences on tumor cells and the immune microenvironment
The role of STAT3 in glioblastoma progression through dual influences on tumor cells and the immune microenvironment
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DOI：
10.1016/j.mce.2017.01.004
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发表时间：
2017-08-15
影响因子：
4.1
通讯作者：
Nam, Do-Hyun
中科院分区：
文献类型：
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作者：
Chang, Nakho;Ahn, Sun Hee;Nam, Do-Hyun
多形性胶质母细胞瘤（GBM）是最具侵袭性的癌症，起源于大脑；一般来说，患者预后不佳，治疗选择有限。信号转导和转录激活因子3 （STAT3）是GBM中肿瘤发生、肿瘤进展和抗肿瘤免疫抑制的关键介质。在很大比例的GBM细胞和肿瘤微环境中，STAT3的持续激活诱导细胞增殖、抗凋亡、胶质瘤干细胞维持、肿瘤侵袭、血管生成和免疫逃逸。这使得STAT3成为GBM的一个有吸引力的治疗靶点和预后指标。靶向STAT3提供了在单个分子中心破坏多个促癌途径的机会。不幸的是，目前在临床试验中还没有成功的STAT3抑制剂。然而，强有力的临床证据表明STAT3是GBM的一个主要因素，证明了确定安全有效的抑制STAT3的策略是正确的。(C) 2017 Elsevier B.V.版权所有
Glioblastoma multiforme (GBM) is the most aggressive form of cancer that begins within the brain; generally, the patient has a dismal prognosis and limited therapeutic options. Signal transducer and activator of transcription 3 (STAT3) is a critical mediator of tumorigenesis, tumor progression, and suppression of anti-tumor immunity in GBM. In a high percentage of GBM cells and tumor microenvironments, persistent activation of STAT3 induces cell proliferation, anti-apoptosis, glioma stem cell maintenance, tumor invasion, angiogenesis, and immune evasion. This makes STAT3 an attractive therapeutic target and a prognostic indicator in GBM. Targeting STAT3 affords an opportunity to disrupt multiple pro-oncogenic pathways at a single molecular hub. Unfortunately, there are no successful STAT3 inhibitors currently in clinical trials. However, strong clinical evidence implicating STAT3 as a major factor in GBM justifies the identification of safe and effective strategies for inhibiting STAT3. (C) 2017 Elsevier B.V. All rights reserved.