PI3K/AKT/mTOR通路
PTEN公司
间质细胞
蛋白激酶B
癌症研究
转染
化学
小RNA
吞噬作用
巨噬细胞
免疫印迹
细胞凋亡
生物
免疫学
体外
基因
生物化学
作者
Boxian Zhao,Wei-guo Zhu
出处
期刊:Journal of Biomaterials and Tissue Engineering
[American Scientific Publishers]
日期:2022-03-01
卷期号:12 (3): 558-563
标识
DOI:10.1166/jbt.2022.2939
摘要
Multiple miRNAs are differentially expressed in gastric cancer (GC). Herein, this study aims to investigate miR-455’s role in GC and its mechanism. Exosomes (exo) separated from BMSCs after transfection were co-cultured with either phagocytes, GC cells (NCI-N87 cell), or macrophages combined with NCI-N87cells (mixed group) followed by analysis of the expression of PTEN, N-cadherin, E-cadherin, and PI3K, and AKT by RT-qPCR and Western blot. Increased miR-455 expression was observed in GC cells upon transfection. GC cells in the mixed group relative to NCI-N87 group exhibited a lower cell migration and invasion and impaired proliferative capacity ( p < 0.05), accompanied with higher expressions of N-cadherin, E-cadherin, PI3K, and AKT, and decreased level of PTEN ( p < 0.05). The combined treatment resulted in a higher phagocytic rate (12.38±0.21%) and phagocytic index (14.29±2.11%) compared to treatment with only phagocytes ( p < 0.05). In conclusion, BMSC-derived exosomal miR-455 inhibits the growth of GC cells and promotes the phagocytosis through inactivating PI3K/AKT signaling pathway.
科研通智能强力驱动
Strongly Powered by AbleSci AI