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中文摘要
翻译
鉴定分子改变和信号异常,启动和
英文摘要
Identification of molecular alterations and signaling abnormalities that initiate and maintain the malignant phenotype in glioblastoma (GBM) is a key step in designing treatment. The NF-¿B and PI3K-Akt pathways are deregulated in GBM and likely to play key roles in the pathogenesis of GBM and in resistance to treatment. NF-¿B activation is a hallmark of inflammation. In this proposal, we aim to characterize the role of the death domain containing kinase receptor interacting protein (RIP, RIP1), in the biology of GBM. RIP1 activates both the NF-¿B and PI3K-Akt pathways in glioma cells. In addition, RIP1 negatively regulates two key tumor suppressor signaling networks, the PTEN and the p53 pathways. RIP1 levels are increased in up to 30% of GBMs but not in Grade II-III gliomas. Furthermore, RIP1 expression confers a worse prognosis in GBM, overexpressing RIP1 induces proliferation of glioma cells and silencing RIP1 inhibits proliferation of glioma cells in an animal model of glioma. The central hypothesis of this proposal is that RIP1 plays a key role in the pathogenesis of GBM and resistance to treatment by regulating key signaling pathways in tumor cells. The broad goal of this proposal is to demonstrate experimentally that RIP1 promotes the malignant phenotype of GBM. In Specific Aim 1, we will explore the mechanistic relationships coupling RIP1 to the proliferation of glioma cells and identify RIP1 specific effector mechanisms influencing proliferation and resistance to chemotherapy in glioma cells. In Specific Aim 2, we will determine the mechanisms and biological significance of RIP1 mediated inhibition of tumor suppressor signaling. In Specific Aim 3 we will benchmark the effect of RIP1 expression in glioma cells using an orthotopic animal model. This study may provide useful insights into the role of inflammation in GBM and help in the design of more effective treatments targeting inflammatory signaling pathways in GBM.
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会议论文
Analysis of Constitutive EGFR Signaling Regulating IRF3 Transcriptional Activity in Cancer Cells.
癌细胞中调节 IRF3 转录活性的组成型 EGFR 信号转导分析。
DOI: 10.1007/978-1-4939-7219-7_14
发表时间: 2017
期刊: Methods in molecular biology (Clifton, N.J.)
影响因子: --
作者: [Guo,Gao, Gong,Ke, Habib,AmynA]
通讯作者: Habib,AmynA
Bimodal EGFR signaling in glioblastoma
  • 批准号:
    10544555
  • 项目类别:
  • 资助金额:
    $41.39万
  • 财政年份:
    2022
  • 负责人:
    AMYN HABIB
  • 依托单位:
Bimodal EGFR signaling in glioblastoma
  • 批准号:
    10363582
  • 项目类别:
  • 资助金额:
    $42.99万
  • 财政年份:
    2022
  • 负责人:
    AMYN HABIB
  • 依托单位:
The role of Nrf2 in mediating resistance to EGFR inhibition in glioblastoma
  • 批准号:
    10404075
  • 项目类别:
  • 资助金额:
    $36.76万
  • 财政年份:
    2020
  • 负责人:
    AMYN HABIB
  • 依托单位:
The role of Nrf2 in mediating resistance to EGFR inhibition in glioblastoma
  • 批准号:
    10615766
  • 项目类别:
  • 资助金额:
    $36.76万
  • 财政年份:
    2020
  • 负责人:
    AMYN HABIB
  • 依托单位:
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