4.7 Article

MiR-145-5p suppresses the proliferation, migration and invasion of gastric cancer epithelial cells via the ANGPT2/NOD_LIKE_RECEPTOR axis

期刊

CANCER CELL INTERNATIONAL
卷 20, 期 1, 页码 -

出版社

BMC
DOI: 10.1186/s12935-020-01483-6

关键词

miR-145-5p; ANGPT2; NOD_LIKE_RECEPTOR; Gastric cancer; Proliferation; Migration and invasion

类别

资金

  1. Key Discipline of Jiaxing Oncology Project [2019-zc-11]
  2. Science and technology project of Jiaxing [2019AY32030]
  3. Jiaxing Key Laboratory of Precision Treatment for Lung Cancer
  4. Key Discipline Established by Zhejiang Province
  5. Jiaxing City Jointly-Pain Medicine [2019-ss-ttyx]

向作者/读者索取更多资源

ObjectiveThis study aimed to investigate the relationship among miR-145-5p, ANGPT2 and the NOD_LIKE_RECEPTOR pathway, thereby revealing the molecular mechanism of these three factors underlying the proliferation, migration and invasion of gastric cancer (GC) epithelial cells.MethodsqRT-PCR was carried out to detect the expression of miR-145-5p and ANGPT2 mRNA. Western blot was performed to test the protein levels of ANGPT2 as well as NOD1, NOD2 and NF-kappa B in the NOD_LIKE_RECEPTOR pathway. The targeting relationship between miR-145-5p and ANGPT2 was verified via a dual-luciferase reporter gene assay. The proliferation, migration and invasion of GC cells were detected through MTT and Transwell assays, respectively.ResultsThe expression of miR-145-5p was significantly down-regulated in GC cells, while that of ANGPT2 was notably up-regulated. MiR-145-5p directly bound with the 3-UTR of ANGPT2 mRNA, thereby targeting ANGPT2 after transcription. Overexpression of miR-145-5p inhibited the proliferation, migration and invasion of GC cells by suppressing ANGPT2. Moreover, low expression of ANGPT2 affected the protein levels of NOD1, NOD2 and NF-kappa B in the NOD_LIKE_RECEPTOR pathway, thus weakening the abilities of cell proliferation, migration and invasion.Conclusions MiR-145-5p plays an important role in GC epithelial cells, and it can affect cell proliferation, migration and invasion of GC cells by targeting ANGPT2 and regulating the NOD_LIKE_RECEPTOR pathway. Overall, our study further elucidates the molecular mechanism underlying the malignant progression of GC.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据