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首页> 外文期刊>Journal of Cellular Physiology >PPAR alpha Antagonist AA452 Triggers Metabolic Reprogramming and Increases Sensitivity to Radiation Therapy in Human Glioblastoma Primary Cells
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PPAR alpha Antagonist AA452 Triggers Metabolic Reprogramming and Increases Sensitivity to Radiation Therapy in Human Glioblastoma Primary Cells

机译：PPARα拮抗剂AA452引发代谢重组,提高灵敏度在初选人类胶质母细胞瘤放疗细胞

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摘要

Glioblastoma (GB) is the most common cancer in the brain and with an increasing incidence. Despite major advances in the field, there is no curative therapy for GB to date. Many solid tumors, including GB, experienced metabolic reprogramming in order to sustain uncontrolled proliferation, hypoxic conditions, and angiogenesis. PPARs, member of the steroid hormone receptor superfamily, are particularly involved in the control of energetic metabolism, particularly lipid metabolism, which has been reported deregulated in gliomas. PPARa was previously indicated by us as a potential therapeutic target for this neoplasm, due to the malignancy grade dependency of its expression, being particularly abundant in GB. In this work, we used a new PPAR alpha antagonist on patient-derived GB primary cells, with particular focus on the effects on lipid metabolism and response to radiotherapy. The results obtained demonstrated that blocking PPARa results in cell death induction, increase of radiosensitivity, and decrease of migration. Therefore, AA452 is proposed as a new adjuvant for the gold standard therapies for GB, opening the possibility for preclinical and clinical trials for this class of compounds. (C) 2016 Wiley Periodicals, Inc.
机译：胶质母细胞瘤(GB)是最常见的癌症大脑和发病率增加。该领域的重大进展,没有治疗治疗GB。包括GB,经验丰富的代谢重编程为了维持控制的增殖,缺氧条件下,血管生成。类固醇激素受体总科,尤其涉及控制能量代谢,尤其是脂类代谢,已报道在神经胶质瘤管制。表示,美国作为一个潜在的治疗目标由于恶性肿瘤,年级依赖的表情,尤其丰富GB。αpatient-derived GB主节点上的对手细胞,特别关注影响脂质代谢和对放疗的反应。获得的结果表明,阻塞PPARa导致细胞死亡感应,增加辐射敏感度,减少迁移。因此,AA452提出了作为一种新的辅助黄金标准的治疗GB,开放临床前和临床的可能性试验这类化合物。威利期刊公司。

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