Effects of miR-141-3p on proliferation, migration and NF-κB signaling pathways in gastric cancer cells
10.3760/cma.j.cn112152-20190625-00395
- VernacularTitle:miR－141－3p对胃癌细胞增殖迁移及核转录因子κB信号通路的影响
- Author:
Fei WANG
1
;
Jixin YANG
;
Zhinian CHEN
Author Information
1. 新乡市中心医院普外二科 453000
- Keywords:
Gastric neoplasms;
MiR-141-3p;
NF-κB signaling pathway;
BGC-823 cells;
Proliferation;
Migration
- From:
Chinese Journal of Oncology
2020;42(7):556-559
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effects of miR-141-3p on proliferation and migration of gastric cancer cells and nuclear factor-κB (NF-κB) signaling pathway.Methods:Human gastric cancer cell line BGC-823 was cultured, and miR-141-3p mimetic (miR-141-3p mimics) was transfected into BGC-823 cells by lipofection. The miR-141-3p overexpressed BGC was constructed. Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect the transfection effect. The proliferation of BGC-823 cells was determined by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Transwell assay was used to detect the effect of miR-141-3p on BGC-823 cell migration. The expressions of NF-κB p65, p-IKK-α and p-IKB-α protein in NF-κB signaling pathway were detected by western blot.Results:Compared with the control group and the negative control group, the expression level of miR-141-3p in BGC-823 cells of the miR-141-3p group was (2.39±0.27), which was higher than (1.00±0.09) of the control group and (1.01±0.10) of the negative control group ( P<0.05). The number of migrating cells in the miR-141-3p group was (47.64±5.65), which was lower than (106.22±12.14) in the control group and (110.40±12.26) in the negative control group ( P<0.05). The expression levels of NF-κB p65, p-IKK-α and p-IKB-α protein in BGC-823 cells were down-regulated ( P<0.05). Conclusion:MiR-141-3p can inhibit the proliferation and migration of human gastric cancer BGC-823 cells, which may be related to the inhibition of NF-κB signaling pathway activation.
