Exploring MicroRNA Expression Profiles Related to the mTOR Signaling Pathway in Mouse Embryonic Fibroblast Cells Treated with Polyethylenimine

Abstract

Although the toxicology of poly(ethylenimine) (PEI) in gene expression levels has been previously investigated, little is known about the effects of PEI on the expression of microRNAs (miRNAs) that regulate gene expression at the post-transcriptional level. In this study, we explored miRNA expression profiles related to cell death mechanisms in mouse embryonic fibroblast (MEF) cells treated with PEI by applying microarray analysis. Based on the analysis of the mTOR signaling pathway, three upregulated miRNAs (mmu-miR-3090-5p, mmu-miR-346-3p, and mmu-miR-494-3p) were verified in MEF cells treated with PEI at 24 h using real-time quantitative reverse transcriptase-polymerase chain reaction. We further demonstrated that these three upregulated miRNAs resulted in the decrease of gene and protein expressions of the target gene growth factor Igf1 in MEF cells treated with PEI or transfected with three upregulated miRNA mimics. However, these three upregulated miRNAs are not all cell-specific. Finally, we demonstrated that the mTOR signaling pathway is inhibited by autophagy induction and that the cell viability decreases in MEF cells treated with PEI or transfected with these three miRNA mimics. Collectively, our data suggested that PEI may affect the regulation of miRNAs in target cells.

Screening circular RNA expression patterns following focal cerebral ischemia in mice

“…In addition, another study found that miR-149-5p, as a tumor suppressor, is associated with cellular migration, proliferation, and apoptosis in renal cell carcinoma [ 30 ]. Furthermore, another previous study indicates that mmu-miR-346-3p regulates cell viability through the mTOR signaling pathway in mouse embryonic fibroblast cells treated with polyethylenimine [ 31 ]. Since mmu_circRNA_40806 is a potential sponge for mmu-miR-20a-3p, we therefore speculate that mmu_circRNA_40806 might competitively bind with mmu-miR-20a-3p and relieve the inhibitory effects on the associated target genes including Hcfc2, Aak1, Capn2, and Tnfsf13b in the network (Figure 7 ).…”

Insulin-like growth factor 1 inhibits autophagy of human colorectal carcinoma drug-resistant cells via the protein kinase B/mammalian target of rapamycin signaling pathway

“…In addition, Troncoso et al ( 11 ) reported that IGF-1 inhibits autophagy via the 5’ adenosine monophosphate-activated protein kinase/mTOR signaling pathway in addition to the AKT/mTOR signaling pathway. It has additionally been reported that inhibition of the mTOR signaling pathway induces autophagy and decreases cell viability ( 17 , 18 ).…”