...
首页> 外文期刊>Journal of molecular histology >Overexpression of leucine aminopeptidase 3 contributes to malignant development of human esophageal squamous cell carcinoma
【24h】

Overexpression of leucine aminopeptidase 3 contributes to malignant development of human esophageal squamous cell carcinoma

机译:亮氨酸氨基肽酶3的过表达有助于人类食管鳞状细胞癌的恶性发展

获取原文
获取原文并翻译 | 示例
           

摘要

Leucine aminopeptidases (LAPs) were associated with tumor cell proliferation, invasion and/or angiogenesis. We aimed to examine the biological function of LAP3 in esophageal squamous cell carcinoma (ESCC). LAP3 expressions were examined in human ESCC tissue and cell lines ECA109 and TE1 cells. Recombinant pSilencer4.1-LAP3-shRNA was transfected into ECA109 cells to silence LAP3 expression. The effects of LAP3 silencing on ECA109 cell proliferation in vitro were evaluated. Flow cytometry profiling was used to detect the differentiate cell cycle distribution in LAP3-silenced ECA109 cells. Wound-healing assay and transwell assay were used to examine the activities of migration and invasion in LAP3-silenced ECA109 cells. We overexpressed LAP3 in TE1 cells to find out the corresponding results. LAP3 expression level was abundance in ESCC tissue. LAP3 silencing significantly reduced ECA109 cell proliferation and colony formation. The knockdown of LAP3 resulted in cell cycle arrest at G1-phase. Moreover, over expression of LAP3 favors TE1 cell proliferation and invasiveness which also confirms its contribution in malignant development. We came to the conclusion that LAP3 contributed to ESCC progression by overcoming cell cycle arrest. The proliferative and migration effects of LAP3 might contribute to malignant development of human ESCC.
机译:亮氨酸氨基肽酶(LAPs)与肿瘤细胞增殖,侵袭和/或血管生成有关。我们旨在检查LAP3在食管鳞状细胞癌(ESCC)中的生物学功能。在人ESCC组织和细胞系ECA109和TE1细胞中检查了LAP3的表达。重组pSilencer4.1-LAP3-shRNA被转染到ECA109细胞中以沉默LAP3表达。评估了LAP3沉默对体外ECA109细胞增殖的影响。流式细胞仪分析用于检测LAP3沉默的ECA109细胞中的分化细胞周期分布。伤口愈合测定法和transwell测定法用于检测沉默了LAP3的ECA109细胞的迁移和侵袭活性。我们在TE1细胞中过表达LAP3,以找出相应的结果。在ESCC组织中LAP3表达水平丰富。 LAP3沉默显着降低ECA109细胞增殖和集落形成。 LAP3的敲低导致细胞周期停在G1期。此外,LAP3的过表达有利于TE1细胞的增殖和侵袭性,这也证实了其在恶性肿瘤发展中的作用。我们得出的结论是,LAP3通过克服细胞周期停滞而促进了ESCC进程。 LAP3的增殖和迁移作用可能有助于人类ESCC的恶性发展。

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