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

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. 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. Firstly, the IC 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. 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.