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首页> 外文学位 >Silibinin Inhibits Glioblastoma Cell Proliferation via AKT/S6/4EBP1 and STAT3 Signaling Pathways In Vitro.
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Silibinin Inhibits Glioblastoma Cell Proliferation via AKT/S6/4EBP1 and STAT3 Signaling Pathways In Vitro.

机译：水飞蓟宾通过AKT / S6 / 4EBP1和STAT3信号通路体外抑制胶质母细胞瘤细胞增殖。

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Background: Glioblastoma is the most common primary and lethal brain tumor in humans. These malignant astrocytic tumors exhibit high proliferation rates and acquire resistance against many therapeutic regimens. Despite aggressive treatment including surgery, radiation, and chemotherapy, the median survival time of 12-15 months after diagnosis has remained unchanged5. Thus, new effective strategies for controlling glioblastoma are required. Because glioblastoma cells like any cancer cells avoid differentiation and apoptosis, the induction of differentiation and apoptosis in glioblastoma cells may be considered as a potential treatment strategy. Silibinin, a natural polyphenolic flavonoid, is a major bioactive component of silymarin, which is isolated from the plant milk thistle. Recent studies have indicated that silibinin has anticancer activities in various cancers including prostate cancer in both in vitro and in vivo models. The underlying mechanisms of this efficacy are still under investigation, but recently an association with the Ca2+/ROS/MAPK dependent mechanism has been proposed46.;Objective: The present study was undertaken to determine the effect of silibinin on glioblastoma cell proliferation in vitro.;Methods: U87MG cells were grown on well tissue culture plates and cell viability was measured by MTT assay. The expression and activity of AKT, S6K, 4EBP1, and STAT3 proteins were measured by Western blot analysis.;Results: Silibinin induced cell death as well as inhibited proliferation in a dose- and time-dependent manner. Accordingly, levels of biologically active phospho-AKT, phospho-S6K, phospho-4EBP1 and phospho-STAT3 were decreased in a dose- and time-dependent manner.;Conclusion: This study demonstrates that silibinin bears an anti-oncogenic property via inhibition of PI3K/AKT and STAT pathways against GBM cells in vitro.
机译：背景：胶质母细胞瘤是人类中最常见的原发性和致死性脑瘤。这些恶性星形细胞肿瘤显示出高增殖率，并且获得了对许多治疗方案的抗性。尽管采取了积极的治疗措施，包括手术，放疗和化疗，但诊断后的中位生存期为12-15个月仍未改变5。因此，需要用于控制胶质母细胞瘤的新的有效策略。由于胶质母细胞瘤细胞像任何癌细胞一样避免分化和凋亡，因此胶质母细胞瘤细胞中诱导分化和凋亡可能被认为是一种潜在的治疗策略。水飞蓟宾是一种天然的多酚类黄酮，是水飞蓟素的主要生物活性成分，水飞蓟素是从植物乳蓟中分离出来的。最近的研究表明，水飞蓟宾在体外和体内模型中均对包括前列腺癌在内的多种癌症具有抗癌活性。该功效的潜在机制仍在研究中，但是最近有人提出了一种与Ca2 + / ROS / MAPK依赖性机制有关的方法。46目的；本研究旨在确定水飞蓟宾对胶质母细胞瘤细胞体外增殖的影响。方法：将U87MG细胞培养在组织培养板上，MTT法检测细胞活力。 Western blot检测AKT，S6K，4EBP1和STAT3蛋白的表达和活性。结果：水飞蓟宾诱导细胞死亡并抑制增殖，并呈剂量和时间依赖性。因此，具有生物活性的磷酸-AKT，磷酸-S6K，磷酸-4EBP1和磷酸STAT3的水平呈剂量和时间依赖性降低。结论：这项研究表明水飞蓟宾通过抑制甲壳素具有抗癌作用。体外针对GBM细胞的PI3K / AKT和STAT途径。

著录项

  • 作者

    Us, Ilkay.;

  • 作者单位

    Long Island University, The Brooklyn Center.;

  • 授予单位 Long Island University, The Brooklyn Center.;
  • 学科 Pharmacology.;Molecular biology.
  • 学位 M.S.
  • 年度 2014
  • 页码 88 p.
  • 总页数 88
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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