• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >The absence of LPA receptor 2 reduces the tumorigenesis by ApcMin mutation in the intestine.
【24h】

The absence of LPA receptor 2 reduces the tumorigenesis by ApcMin mutation in the intestine.

机译：LPA受体2的缺失会降低肠道中ApcMin突变引起的肿瘤发生。

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

Lysophosphatidic acid (LPA) is a lipid mediator that mediates several effects that promote cancer progress. The LPA receptor type 2 (LPA(2)) expression is often elevated in several types of cancers, including colorectal cancer (CRC). In this study, we investigated the role of LPA(2) in the development of intestinal adenomas by comparing Apc(Min/+) mice with Apc(Min/+)/Lpar2(-/-) mice. There were 50% fewer intestinal adenomas in Apc(Min/+)/Lpar2(-/-) mice than Apc(Min/+) mice. Smaller-size adenomas (<1 mm) were found at higher frequencies in Apc(Min/+)/Lpar2(-/-) mice compared with Apc(Min/+) mice at the two age groups examined. The expression level of LPA(2) correlated with increased size of intestinal adenomas. Reduced tumor multiplicity and size in Apc(Min/+)/Lpar2(-/-) mice correlated with decreased proliferation of intestinal epithelial cells. Apc(Min/+)/Lpar2(-/-) mice showed an increased level of apoptosis, suggesting that LPA(2)-mediated signaling stimulates intestinal tumor development and progress by regulating both cell proliferation and survival. In addition, the expression levels of Krupple-like factor 5 (KLF5), beta-catenin, cyclin D1, c-Myc, and hypoxia-inducible factor-1alpha (HIF-1alpha) were significantly altered in Apc(Min/+)/Lpar2(-/-) mice compared with Apc(Min/+) mice. In vitro studies using HCT116 cells showed that LPA induced cyclin D1, c-Myc, and HIF-1alpha expression, which was attenuated by knockdown of LPA(2). In summary, intestinal tumor initiated by Apc mutations is altered by LPA(2)-mediated signaling, which regulates tumor growth and survival by altering multiple targets.
机译：溶血磷脂酸（LPA）是一种脂质介质，可介导促进癌症进展的多种作用。 LPA 2型受体（LPA（2））表达在几种类型的癌症（包括结直肠癌（CRC））中通常升高。在这项研究中，我们通过比较Apc（Min / +）小鼠与Apc（Min / +）/ Lpar2（-/-）小鼠来研究LPA（2）在肠腺瘤发展中的作用。与Apc（Min / +）小鼠相比，Apc（Min / +）/ Lpar2（-/-）小鼠的肠腺瘤少50％。在两个年龄组中，与Apc（Min / +）小鼠相比，Apc（Min / +）/ Lpar2（-/-）小鼠中发现较高频率的较小腺瘤（<1 mm）。 LPA（2）的表达水平与肠腺瘤的大小增加相关。 Apc（Min / +）/ Lpar2（-/-）小鼠的肿瘤多样性和大小减少与肠道上皮细胞增殖减少有关。 Apc（Min / +）/ Lpar2（-/-）小鼠显示出增加的凋亡水平，表明LPA（2）介导的信号传导通过调节细胞增殖和存活来刺激肠道肿瘤的发生和发展。此外，Apc（Min / +）/中，Krupple样因子5（KLF5），β-catenin，cyclin D1，c-Myc和缺氧诱导因子1alpha（HIF-1alpha）的表达水平显着改变。 Lpar2（-/-）小鼠与Apc（Min / +）小鼠相比。使用HCT116细胞进行的体外研究表明，LPA诱导了细胞周期蛋白D1，c-Myc和HIF-1alpha的表达，该表达被LPA（2）的敲低减弱了。总之，LPC（2）介导的信号传导可改变由Apc突变引发的肠道肿瘤，该信号通过改变多个靶标来调节肿瘤的生长和存活。

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