• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >RelB NF-κB Represses Estrogen Receptor α Expression via Induction of the Zinc Finger Protein Blimp1
【24h】

RelB NF-κB Represses Estrogen Receptor α Expression via Induction of the Zinc Finger Protein Blimp1

机译：RelBNF-κB通过诱导锌指蛋白Blimp1抑制雌激素受体α表达。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Aberrant constitutive expression of NF-κB subunits, reported in more than 90% of breast cancers and multiple other malignancies, plays pivotal roles in tumorigenesis. Higher RelB subunit expression was demonstrated in estrogen receptor alpha (ERα)-negative breast cancers versus ERα-positive ones, due in part to repression of RelB synthesis by ERα signaling. Notably, RelB promoted a more invasive phenotype in ERα-negative cancers via induction of the BCL2 gene. We report here that RelB reciprocally inhibits ERα synthesis in breast cancer cells, which contributes to a more migratory phenotype. Specifically, RelB is shown for the first time to induce expression of the zinc finger repressor protein Blimp1 (B-lymphocyte-induced maturation protein), the critical mediator of B- and T-cell development, which is transcribed from the PRDM1 gene. Blimp1 protein repressed ERα (ESR1) gene transcription. Commensurately higher Blimp1/PRDM1 expression was detected in ERα-negative breast cancer cells and primary breast tumors. Induction of PRDM1 gene expression was mediated by interaction of Bcl-2, localized in the mitochondria, with Ras. Thus, the induction of Blimp1 represents a novel mechanism whereby the RelB NF-κB subunit mediates repression, specifically of ERα, thereby promoting a more migratory phenotype.
机译：超过90％的乳腺癌和其他多种恶性肿瘤中都报告了NF-κB亚基的异常组成型表达，在肿瘤发生中起着关键作用。与雌激素受体阳性的乳腺癌相比，雌激素受体α（ERα）阴性的乳腺癌中RelB亚基的表达更高，部分原因是通过ERα信号转导抑制了RelB的合成。值得注意的是，RelB通过诱导 BCL2 基因在ERα阴性癌症中促进了更具侵袭性的表型。我们在这里报告，RelB相互抑制乳腺癌细胞中的ERα合成，这有助于更迁移的表型。具体来说，RelB首次显示出诱导锌指阻遏蛋白Blimp1（B淋巴细胞诱导的成熟蛋白）的表达，Blimp1是B细胞和T细胞发育的关键介质，是从 PRDM1转录而来的基因。 Blimp1蛋白抑制ERα（ ESR1 ）基因的转录。在ERα阴性乳腺癌细胞和原发性乳腺肿瘤中检测到相应的Blimp1 / PRDM1 表达更高。 PRem1 基因表达的诱导是通过位于线粒体中的Bcl-2与Ras相互作用介导的。因此，Blimp1的诱导代表了一种新的机制，其中RelBNF-κB亚基介导了抑制，特别是ERα的抑制，从而促进了更多的迁移表型。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号