| Literature DB >> 31949768 |
Qi Chen1, Yugao Zhang2, Liping Xu3.
Abstract
Gastric cancer is a serious threat to human health, and its pathogenesis may be regulated by a variety of mRNAs. Abnormal expression of microRNA-340 has been frequently reported in many malignant neoplasms, while the molecular mechanism of miR-340 has not been explored in gastric cancer. In this study, the mRNA level of miR-340 was determined by real-time PCR in GC cell lines. The miR-340 mimic was transiently transfected into GC cells by using Lipofectamine™ 2000 reagent. The BrdU-ELISA results showed that introduction of miR-340 inhibited cell proliferation. It was demonstrated that miR-340 mimic arrested cell cycle progression and promoted apoptosis of MKN-45 and BGC-823 cells. In addition, the overexpression of miR-340 could inhibit invasion and EMT of MKN-45 and BGC-823 cells. The expression of NF-κB1 was evidently reduced by up-regulation of miR-340. Luciferase reporter assay further confirmed that miR-340 could directly target the 3'UTR of NF-κB1. Moreover, overexpression of NF-κB1 transfected with miR-340 mimic partially reversed the inhibitory of miR-340 mimic in MKN-45 and BGC-823 cells. In conclusion, miR-340 induced cell apoptosis and inhibited invasion by down-regulation of NF-κB1, which might be a potential target in treatment and prevention of gastric cancer. IJCEPEntities:
Keywords: NF-κB1; gastric cancer; invasion; microRNA-340; proliferation
Year: 2018 PMID: 31949768 PMCID: PMC6962829
Source DB: PubMed Journal: Int J Clin Exp Pathol ISSN: 1936-2625