• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国政府科技报告 >Androgenic Regulation of White Adipose Tissue-Prostate Cancer Interactions.
【24h】

Androgenic Regulation of White Adipose Tissue-Prostate Cancer Interactions.

机译：白色脂肪组织 - 前列腺癌相互作用的雄激素调节。

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

摘要

Glipr1 (mouse)/GLIPR1 (human) is a direct p53 target gene that encodes a member of the pathogenesis-related protein family. This 28-kDa protein has a putative signal peptide sequence and a transmembrane domain suggesting extracellular functional activity. We have shown that Glipr1/GLIPR1 functions as a tumor suppressor through proapoptotic signaling in prostate cancer and potentially other malignancies. We recently discovered that recombinant Glipr1/GLIPR1 protein (rGlipr1/rGLIPR1) treatment results in growth arrest/apoptotic cell death in multiple prostate cancer cell lines in vitro. Further preclinical studies using PC-3 xenograft models demonstrated that rGLIPR1 suppressed PC-3 tumor growth when administered intratumorally or intraperitoneally. Although the direct growth suppressor/pro-apoptotic activities of Glipr1/GLIPR1 are now established, the physiological functions of GLIPR1 remain largely unknown. To further study Glipr1/GLIPR1 protein functions we generated mice harboring a targeted inactivation of the Glipr1 gene. We discovered that the wet weight of Glipr1 KO male white adipose tissue (WAT) was increased compare to the Glipr+/+ male littermates (Glipr1 WT). Based on these initial observations we pursued additional experiments. Overall, our preliminary data indicate that, in addition to direct growth suppressor/pro-apoptotic activities of Glipr1/GLIPR1 in prostate cancer cells, testosterone stimulated, prostate derived serum Glipr1/GLIPR1 is a hormone that can inhibit WAT function, including suppression of leptin secretion. Increased serum leptin levels may promote prostate cancer progression. We propose to study gene expression in the WAT and prostate tissues of Glipr1 WT and Glipr1 KO animals to characterize the genetic pathways that are affected by the presence or absence of Glipr1.

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