...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Signalling >SIPAR negatively regulates STAT3 signaling and inhibits progression of melanoma
【24h】

SIPAR negatively regulates STAT3 signaling and inhibits progression of melanoma

机译：SIPAR负调节STAT3信号传导并抑制黑素瘤进展

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Persistently activated STAT3 is important for tumorigenesis in a variety of cancers, including melanoma. Although many co-factors in the regulation of STAT3 activity have been identified, it remains unclear how STAT3 phosphorylation is negatively regulated. Here, we report that SIPAR (STAT3. Interacting Protein As a Repressor) inhibits STAT3 activity by accelerating its dephosphorylation. We observed that SIPAR directly interacted with STAT3 upon IL-6 stimulation. Moreover, over-expression of SIPAR reduced, whereas depletion enhanced, the level of phosphorylated STAT3. We further demonstrated that SIPAR inhibited the growth of melanoma cells by decreasing the level of phosphorylated STAT3 and the expression of its target genes. These results suggest that SIPAR, functioning as a new negative regulator, inhibits STAT3 activity by enhancing its dephosphorylation and represses melanoma progression.
机译：持续激活的STAT3对于包括黑色素瘤在内的多种癌症的肿瘤发生都很重要。尽管已经鉴定出许多调节STAT3活性的辅助因子，但仍不清楚如何对STAT3的磷酸化进行负调控。在这里，我们报道SIPAR（STAT3。相互作用蛋白作为阻遏物）通过加速STAT3的去磷酸化来抑制STAT3的活性。我们观察到，IL-6刺激后SIPAR直接与STAT3相互作用。此外，SIPAR的过表达减少了磷酸化STAT3的水平，而耗竭则增加了。我们进一步证明，SIPAR通过降低磷酸化STAT3的水平及其靶基因的表达来抑制黑素瘤细胞的生长。这些结果表明，SIPAR作为一种新的负调节剂，可通过增强STAT3的去磷酸化来抑制STAT3的活性并抑制黑色素瘤的进展。

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