Long non-coding RNAs (lncRNAs) have been largely reported to contribute to the development and progression of abdominal aortic aneurysm (AAA), a common vascular degenerative disease. The present study was set out with the aim to investigate the possible role of lncRNA Sox2ot in the development of AAA. In this study, we found that lncRNA Sox2ot and early growth response factor-1 (Egr1) were highly expressed, while microRNA (miR)-145 was poorly expressed in Ang II-induced AAA mice and oxidative stress-provoked vascular smooth muscle cell (VSMC) model. Egr1 was a potential target gene of miR-145, and lncRNA Sox2ot could competitively bind to miR-145 to upregulate Egr1 expression. Overexpression of miR-145-5p was found to attenuate oxidative stress and inflammation by inhibiting Egr1 both
in vivo
and
in vitro
, which was counteracted by lncRNA Sox2ot. Taken together, the present study provides evidence that downregulation of lncRNA Sox2ot suppressed the expression of Egr1 through regulating miR-145, thus inhibiting the development of AAA, highlighting a theoretical basis for AAA treatment.
MicroRNAs (miRNAs) have been reported to serve pivotal roles in the regulation of papillary thyroid cancer (PTC) development; thus, the aim of this study is to identify the impact of miR-203 and AKT3 on the epithelial-mesenchymal transition (EMT), migration and invasion of PTC. MiR-203 and AKT3 expression in PTC tissues and cells were tested. TPC-1 cells and K1 cells were screened for follow-up experiments. Apoptosis-related proteins (Bcl-2 and Bax), EMT-related proteins (Vimentin and E-cadherin), proliferation-associated proteins (Ki67 and CDK4), invasion-and migration-related protein (MMP-2 and MMP-9) were verified. The effects of upregulated miR-203 and downregulated AKT3 on the biological characteristics of PTC cells in each group were detected via the gain-and loss-of-function assays. The targeting relationship between miR-203 and AKT3 was verified.MiR-203 expression declined and AKT3 heightened in PTC tissues and cells. Upregulated miR-203 and downregulated AKT3 reduced the tumor volume and weight, suppressed cell migration, colony formation, proliferation, invasion, proliferation-associated proteins (Ki67 and CDK4), invasion-and migration-related protein (MMP-2 and MMP-9) and promoted cell apoptosis, raised E-cadherin and decreased Vimentin protein expression in TPC-1 cells. On the contrary, the K1 cells with the downregulated miR-203 or upregulated AKT3 exhibited an opposite result. This study suggests that upregulated miR-203 suppresses EMT, invasion, proliferation and migration as well as induces apoptosis of PTC cells via downregulated AKT3.
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