Journal
CANCER CELL INTERNATIONAL
Volume 20, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s12935-020-01483-6
Keywords
miR-145-5p; ANGPT2; NOD_LIKE_RECEPTOR; Gastric cancer; Proliferation; Migration and invasion
Categories
Funding
- Key Discipline of Jiaxing Oncology Project [2019-zc-11]
- Science and technology project of Jiaxing [2019AY32030]
- Jiaxing Key Laboratory of Precision Treatment for Lung Cancer
- Key Discipline Established by Zhejiang Province
- Jiaxing City Jointly-Pain Medicine [2019-ss-ttyx]
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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.
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