miR-214-3p promotes the proliferation, migration and invasion of osteosarcoma cells by targeting CADM1
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Updated: Feb 7, 2026

In Vitro Assays to Evaluate the Migration, Invasion, and Proliferation of Immortalized Human First-trimester Trophoblast Cell Lines
Published on: March 5, 2019
Haiqing Cai1, Mingyuan Miao1, Zhigang Wang1
1Pediatric Orthopedic Department, Shanghai Children's Medical Center, Shanghai Jiaotong University School of Medicine, Shanghai 200031, P.R. China.
Abstract:
Although osteosarcoma (OS) is the most common type of primary bone tumor in adolescents and young adults, its mechanism remains unclear. A previous study by the authors demonstrated that miR-214-3p was upregulated in OS patients. Therefore, the present study aimed to investigate the effect and molecular mechanism of miR-214-3p in OS cells. OS cell lines, U2OS and MNNG/HOS Cl#5, were transiently transfected with miR-214-3p mimics, a control mimic, miR-214-3p inhibitors and a control inhibitor. Subsequent assays revealed that elevated miR-214-3p promoted the proliferative, migratory and invasive abilities of OS cells, while the opposite effects were observed in cells that were transfected with miR-214-3p inhibitors. The interaction between miR-214-3p and cell adhesion molecule 1 (CADM1) 3'untranslated region (UTR) was verified by a dual luciferase assay, which indicated that the relative luciferase activity was decreased in 293T cells that were co-transfected with miR-214-3p mimic and psiCHECK2-CADM1-3'UTR compared with cells that were co-transfected with psiCHECK2-CADM1-3'UTR and control mimic. The knockdown of CADM1 using small-interfering RNA enhanced the proliferative, migratory and invasive abilities of OS cells. Furthermore, downregulated CADM1 expression increased the expression of phosphorylated P44/42 mitogen activated kinase (MAPK). In conclusion, miR-214-3p was able to directly target CADM1 and decrease its expression. This resulted in the activation of the P44/42 MAPK signaling pathway, and thereby promoted the proliferation, migration and invasion of OS cells.
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