Dual luciferase reporter assay was performed to identify the relationships between miR-216b and FoxM1. qRT-PCR results revealed that miR-216b expression was significantly downregulated, and FoxM1 was observed to be significantly upregulated in human OS cell lines (MG-63) and tissues.
MEG3 and miR-361-5p were observed to be significantly downregulated within both osteosarcoma tissues and cell lines, whereas FoxM1 was upregulated in osteosarcoma tissues and cell lines (p < 0.05).
In addition, the AKT pathway activation promoted TUG1 expression by upregulating the expression of FOXM1, forming a positive feedback loop in osteosarcoma.
Similar to FOXM1, critical components of the Wnt signaling pathway, including β-catenin, c-Myc, and Cyclin D1, were also highly expressed in different human osteosarcoma cells lines.
Experiments were performed to determine the effects of WIN on proliferation, cell cycle distribution, and programmed cell death in human osteosarcoma MG63 and Saos-2 cells.
Here, we show that both early-passage Foxm1(-)(/)(-) mouse embryonic fibroblasts (MEFs) and human osteosarcoma U2OS cells depleted of FoxM1 protein by small interfering RNA fail to grow in culture due to a mitotic block and accumulate nuclear levels of cyclin-dependent kinase inhibitor (CDKI) proteins p21(Cip1) and p27(Kip1).
Furthermore, we demonstrated that conditional overexpression of Foxm1b protein in osteosarcoma U2OS cells greatly enhances anchorage-independent growth of cell colonies on soft agar.