Cardiovascular disease is the leading cause of death worldwide. Dysregulation of microRNAs (miRNAs) has been found to be associated with cardiovascular diseases such as atherosclerosis. In the present study, we examined the role of miR-147b in the proliferation and migration of vascular smooth muscle cells (VSMCs). Quantitative real-time PCR was performed to determine the expression levels of miR-147b and Yin Yang 1 (YY1) mRNA. CCK-8, transwell migration and wound healing assays were used to determine cell proliferation and migration of VSMCs, respectively. Luciferase reporter assay confirmed the downstream target of miR-147b. The protein level of YY1 was measured by western blot analysis. Platelet-derived growth factor-bb (PDGF-bb) treatment promoted cell proliferation and increased miR-147b expression in VSMCs. Overexpression of miR-147b enhanced cell proliferation and migration of VSMCs, while knock-down of miR-147b suppressed cell proliferation and migration of VSMCs or PDGF-bb-treated VSMCs. Further, bioinformatics prediction and luciferase reporter assay showed that YY1 was a downstream target of miR-147b, and miR-147b negatively regulated the mRNA and protein expression of YY1 in VSMCs. Overexpression of YY1 inhibited cell proliferation and migration of VSMCs and attenuated the effects of miR-147b overexpression on cell proliferation and migration. In addition, overexpression of miR-147b increased the Wnt/β-catenin signaling activities in VSMCs. In conclusion, our results suggest that miR-147b plays important roles in the control of cell proliferation and migration of VSMCs possibly via targeting YY1.

Esophageal squamous cell carcinoma (ESCC) is one of the most aggressive types of cancer worldwide, with a poor prognosis. The aim of the present study was to investigate the effect of cisatracurium (Cis) on epithelial-to-mesenchymal transition (EMT) in ESCC and its potential mechanism of action. In the present study, Cis was used to treat ECA-109 cells, with cell proliferation measured by a Cell Counting Kit-8 assay and the expression of TGF-β and phospho-Smad2/3 detected by western blotting. TGF-β was then applied to induce EMT. Flow cytometry, wound healing and Transwell assays were used to evaluate cell proliferation, apoptosis, invasion and migration. In addition, cell cycle-related proteins, including cyclin D1, p53 and p21, and EMT-associated proteins, including E-cadherin (E-cad), N-cadherin (N-cad), Vimentin and Slug, were examined by western blot analysis. The results revealed that Cis inhibited the proliferation and promoted apoptosis of ESCC cells. Following treatment with Cis, the expression of TGF-β and phosphorylation of Smad2/3 were downregulated. Cis also suppressed cancer cell invasion and migration induced by TGF-β. In addition, the expression levels of cyclin D1 were decreased, accompanied by increased p53 and p21 expression. In addition, the expression level of E-cad was increased, whereas N-cad, Vimentin and Slug were significantly reduced. Taken together, the results of the present study revealed that exposure of ESCC cells to Cis inhibited EMT and reduced cell invasion and metastasis through the TGF-β/Smad signaling pathway.