Death receptors in prostate cancer biology and apoptosis

前列腺癌生物学和细胞凋亡中的死亡受体

基本信息

  • 批准号:
    6384220
  • 负责人:
  • 金额:
    $ 15.2万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2001
  • 资助国家:
    美国
  • 起止时间:
    2001-07-01 至 2003-06-30
  • 项目状态:
    已结题

项目摘要

DESCRIPTION (provided by applicant): The main goals of this proposal is to explore the role of membrane death receptors and their ligands in nonsteroidal anti-inflammatory drugs (NSAIDs) and ionizing radiation (IR)-induced apoptosis in human prostate cancer cells. Evidence suggests that the regular use of NSAIDs reduces the risk of other cancer types but their role in prevention of prostate cancer has not been elucidated. NSAIDs are believed to mediate their chemopreventive and anti-tumorigenic effects by inducing apoptosis. IR is an important therapeutic modality against prostate cancer and is believed to kill prostate cancer cells by inducing apoptosis. However, the biochemical and molecular pathways via which these agents induce apoptosis have not been fully elucidated. Preliminary results presented in this proposal indicate that sulindac sulfide, a clinically relevant NSAID, induces apoptosis in human prostate cancer cells. Sulindac sulfide also augments ionizing radiation (IR)-induced apoptosis in human prostate cancer cells. Preliminary evidence presented in this application further suggests that death receptor 5 (DR5) may be involved in transducing the apoptotic signals of sulindac sulfide and IR. Thus, the role of DR5 and its ligand in this context will be explored. Similarly, the contribution of other death receptors and their ligands in sulindac sulfide, IR and sulindac sulfide+IR-mediated apoptosis will be investigated. DR5 activation stimulates apoptotic pathway and NF-kB-dependent survival pathway. IR activates NF-kB while sulindac is known to inhibit NF-kB. Thus, the role of NF-kB in sulindac sulfide-induced radiosensitization will also be explored. The long-term objectives of this proposal are to (i) better understand the apoptotic signaling pathways in human prostate cancer cells and (ii) lay the ground work to potentially develop a novel treatment and/or prevention strategy against this deadly disease.
描述(由申请人提供):本提案的主要目标是

项目成果

期刊论文数量(0)
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M. SAEED SHEIKH其他文献

M. SAEED SHEIKH的其他文献

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{{ truncateString('M. SAEED SHEIKH', 18)}}的其他基金

Development of dihydroartemisinin as a novel preventive agent for prostate cancer
双氢青蒿素作为前列腺癌新型预防剂的开发
  • 批准号:
    8050362
  • 财政年份:
    2011
  • 资助金额:
    $ 15.2万
  • 项目类别:
Development of dihydroartemisinin as a novel preventive agent for prostate cancer
双氢青蒿素作为前列腺癌新型预防剂的开发
  • 批准号:
    8242022
  • 财政年份:
    2011
  • 资助金额:
    $ 15.2万
  • 项目类别:
A novel biomarker and therapeutic target for breast cancer
乳腺癌的新型生物标志物和治疗靶点
  • 批准号:
    8220835
  • 财政年份:
    2011
  • 资助金额:
    $ 15.2万
  • 项目类别:
A novel biomarker and therapeutic target for breast cancer
乳腺癌的新型生物标志物和治疗靶点
  • 批准号:
    8062885
  • 财政年份:
    2011
  • 资助金额:
    $ 15.2万
  • 项目类别:
Characterization of a novel stress-regulated anti-apoptotic ubiquitin ligase
新型应激调节抗凋亡泛素连接酶的表征
  • 批准号:
    7466107
  • 财政年份:
    2008
  • 资助金额:
    $ 15.2万
  • 项目类别:
Characterization of a novel stress-regulated anti-apoptotic ubiquitin ligase
新型应激调节抗凋亡泛素连接酶的表征
  • 批准号:
    7567486
  • 财政年份:
    2008
  • 资助金额:
    $ 15.2万
  • 项目类别:
PDRG, a novel p53 and DNA damage-regulated gene and colorectal cancer
PDRG,一种新型 p53 和 DNA 损伤调节基因与结直肠癌
  • 批准号:
    7265025
  • 财政年份:
    2007
  • 资助金额:
    $ 15.2万
  • 项目类别:
PDRG, a novel p53 and DNA damage-regulated gene and colorectal cancer
PDRG,一种新型 p53 和 DNA 损伤调节基因与结直肠癌
  • 批准号:
    7426429
  • 财政年份:
    2007
  • 资助金额:
    $ 15.2万
  • 项目类别:
Characterization:novel genotoxic stress-regulated gene
表征:新型遗传毒性应激调节基因
  • 批准号:
    7030099
  • 财政年份:
    2006
  • 资助金额:
    $ 15.2万
  • 项目类别:
Characterization:novel genotoxic stress-regulated gene
表征:新型遗传毒性应激调节基因
  • 批准号:
    7229934
  • 财政年份:
    2006
  • 资助金额:
    $ 15.2万
  • 项目类别:

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  • 批准号:
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  • 财政年份:
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