Baicalein inhibits cell development, metastasis and EMT and induces apoptosis by regulating ERK signaling pathway in osteosarcoma.

Background: Osteosarcoma is a highly malignant primary tumor. Baicalein has broad-spectrum anti-tumor effects. This study aimed to study the specific molecular regulatory mechanism of baicalein in anti-osteosarcoma and the possible regulatory signaling network involved.Methods: In vitro experiment, MG-63 cells treated with 0, 50, 75, and 100 μM of baicalein. Cell viability, proliferation, migration, invasion, cycle, apoptosis, and morphology were detected using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazoliumbromide (MTT), clone formation, wound healing, Transwell, flow cytometry, Hoechst staining, wound healing and microscopic observation. In addition, cycle, apoptosis and EMT-related proteins and p-ERK/ERK expression level were analyzed using western blotting. In vivo experiments were performed by BALB/c-nude mice model establishment to detect mice and tumor weight, tumor volume, positive rate and p-ERK/ERK expression when mice treated with 100 μM of baicalein.Results: Firstly, the IC50 of baicalein was 67.57 μM. Then, baicalein decreased cell viability, proliferation, migration, invasion, and the expression of CDK2, Cyclin D1, Cyclin E1, Bcl-2, N-cad, Vimentin, MMP-2, MMP-9, p-ERK/ERK, while increased G1 phase numbers, apoptosis and the expression level of p21, p27, cleaved caspase 3/9, Bax, E-cad, ZO-1 in a dose-dependent manner in MG-63 cells. Also, baicalein reduced the body weight, tumor weight and volume and relative expression level of p-ERK/ERK in vivo.Conclusion: Baicalein inhibits cell development, metastasis, and EMT progress and induces cell cycle arrest and apoptosis by regulating ERK signaling pathway in osteosarcoma, and has a visible anti-osteosarcoma effect in vivo.