Role of cytokine-inducible transcription factors in renal cell carcinoma

细胞因子诱导转录因子在肾细胞癌中的作用

基本信息

  • 批准号:
    15591715
  • 负责人:
  • 金额:
    $ 2.18万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    2003
  • 资助国家:
    日本
  • 起止时间:
    2003 至 2004
  • 项目状态:
    已结题

项目摘要

Renal cell carcinoma(RCC) is occasionally associated with paraneoplastic syndromes such as inflammatory reactions and leukocytosis. Cytokines produced by cancer cells are considered to accelerate cell growth in an autocrine or paracrine manner as well as induce cahexic reactions to the host. Furtheremore, Cytokine-dependent signal transduction has been implicated to play a role in maintaining cancer cell survival. Therefore, blocking the signal pathways may have a therapeutic potential for RCC. Transcription factors not only induce de novo cytokine expression, but their activities are also induced by cytokines and therefore may play a substantial role in cytokine-mediated autocrine growth in RCC. Increased activation of NF-κB, STAT3 and C/EBP-β were associated with a high tumor stage and grade. PI3K-Akt pathway has been implicated to regulate key effector molecules involved in controlling the balance of cell survival and apoptosis. Akt activation determined by immunohistochemistry associated with high tumor grade and metastatic disease. Immunoblotting studies revealed decreased PTEN expression is necessary but not sufficient for Akt activation. Akt inhibitor induced apoptosis in some RCC cell lines. MAP kinases include ERKs, JNK, and p38. ERKs are constitutively activated, but JNK and p38 are inactivated in a steady state of RCC. ERKs inactivation did not induce apoptosis, therfore, ERKs do not seem to relate to cell survival. In contrast, inductive JNK or p38 activation induced apoptosis in some RCC cell lines. Our investigation of signal transduction pathways shed some light on a potential novel treatment for RCC. These signal trasduction molecules mentioned above are candidates for molecular targeting therapy for RCC.
肾细胞癌(RCC)有时与副肿瘤综合征相关,如炎症反应和白细胞增多。癌细胞产生的细胞因子被认为以自分泌或旁分泌的方式加速细胞生长,并诱导对宿主的己型反应。此外,细胞因子依赖的信号转导被认为在维持癌细胞存活方面发挥了作用。因此,阻断信号通路可能对肾癌有治疗潜力。转录因子不仅诱导新生细胞因子的表达,而且其活性也受细胞因子的诱导,因此可能在细胞因子介导的肾癌自分泌生长中发挥重要作用。NF-κB、STAT3和C/EBP-β的活性升高与肿瘤的分期和分级有关。PI3K-Akt信号转导通路参与调控细胞存活与凋亡平衡的关键效应分子。免疫组织化学方法检测AKT活性与肿瘤高分级及转移相关。免疫印迹研究表明,降低PTEN的表达是Akt激活所必需的,但不是充分的。AKT抑制剂可诱导部分肾癌细胞发生凋亡。MAP激酶包括ERKs、JNK和p38。ERKs是结构性激活的,而JNK和p38在RCC的稳定状态下失活。ERKs失活不能诱导细胞凋亡,因此ERKs似乎与细胞存活无关。相反,诱导性JNK或p38激活可诱导某些肾癌细胞系发生凋亡。我们对信号转导通路的研究为肾癌的潜在新治疗提供了一些线索。上述信号转导分子是肾癌分子靶向治疗的候选分子。

项目成果

期刊论文数量(26)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Oya M, Takayanagi A, Horiguchi A, Mizuno M, Ohtsubo M, Marumo K, Shimizu N, Murai M.: "Increased nuclear factor-κB activation is related to the tumor development of renal cell carcinoma."Carcinogenesis. 24・3. 377-384 (2003)
Oya M、Takayanagi A、Horiguchi A、Mizuno M、Ohtsubo M、Marumo K、Shimizu N、Murai M.:“核因子-κB 激活增加与肾细胞癌的肿瘤发展有关。”癌发生 24・3。 377-384 (2003)
  • DOI:
  • 发表时间:
  • 期刊:
  • 影响因子:
    0
  • 作者:
  • 通讯作者:
Increased activation of CCAAT/enhancer binding protein-β correlates with the invasiveness of renal cell carcinoma.
CCAAT/增强子结合蛋白-β 的激活增加与肾细胞癌的侵袭性相关。
  • DOI:
  • 发表时间:
    2003
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Oya;M.;Horiguchi;A.;Mizuno;M.;Marumo;K.;Murai;M.
  • 通讯作者:
    M.
Increased nuclear factor-κB activation is related to the tumor development of renal cell carcinoma
  • DOI:
    10.1093/carcin/24.3.377
  • 发表时间:
    2003-03-01
  • 期刊:
  • 影响因子:
    4.7
  • 作者:
    Oya, M;Takayanagi, A;Murai, M
  • 通讯作者:
    Murai, M
Elevated Akt activation and its impact on clinicopathological features of renal cell carcinoma
  • DOI:
    10.1016/s0022-5347(05)63998-5
  • 发表时间:
    2003-02-01
  • 期刊:
  • 影响因子:
    6.6
  • 作者:
    Horiguchi, A;Oya, M;Murai, M
  • 通讯作者:
    Murai, M
Inhibition of MKP-1 expression potentiates JNK related apoptosis in renal cancer cells
  • DOI:
    10.1097/01.ju.0000124990.37563.00
  • 发表时间:
    2004-08-01
  • 期刊:
  • 影响因子:
    6.6
  • 作者:
    Mizuno, R;Oya, M;Murai, M
  • 通讯作者:
    Murai, M
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OYA Mototsugu其他文献

OYA Mototsugu的其他文献

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{{ truncateString('OYA Mototsugu', 18)}}的其他基金

Development of novel therapeutic modality by integrated analysis of immune environment of renal cell carcinoma and remodeling after inhibition of angiogenesis
综合分析肾细胞癌的免疫环境和抑制血管生成后的重塑,开发新的治疗模式
  • 批准号:
    18H02939
  • 财政年份:
    2018
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Elucidation of molecular targets based on epithelial-mesenchymal transition for the treatment of renal cell carcinoma
阐明基于上皮间质转化的肾细胞癌治疗分子靶点
  • 批准号:
    24390374
  • 财政年份:
    2012
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Microenviroment and organ specific metastases in urological cancers as tools to elucidate molecular mechanism of carcinogenesis and tumor development.
泌尿系统癌症中的微环境和器官特异性转移作为阐明癌发生和肿瘤发展分子机制的工具。
  • 批准号:
    21390445
  • 财政年份:
    2009
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Hypoxia responsiveness in renal cell carcinoma
肾细胞癌的缺氧反应
  • 批准号:
    17591701
  • 财政年份:
    2005
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Genetic analysis of multiple sproradic renal call carcinoma
多发性肾癌的基因分析
  • 批准号:
    12671555
  • 财政年份:
    2000
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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对 RIPK1 依赖性死亡的敏感性作为增强肾细胞癌 (RCC) 对免疫治疗反应的策略
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