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Journal of Environmental Pathology, Toxicology and Oncology

Impact factor: 1.246

ISSN Print: 0731-8898
ISSN Online: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.2015011925
pages 85-93

(−)-Epigallocatechin-3-gallate inhibits osteosarcoma cell invasiveness by inhibiting the MEK/ERK signaling pathway in human osteosarcoma cells

Guoqing Tang
Orthopedic Center, Kunshan Hospital of Traditional Chinese Medicine, Kunshan, China
Zhengshi Zhang
Orthopedic Center, Kunshan Hospital of Traditional Chinese Medicine, Kunshan, China
Hongbin Qian
Orthopedic Center, Kunshan Hospital of Traditional Chinese Medicine, Kunshan, China
Ji Chen
Orthopedic Center, Kunshan Hospital of Traditional Chinese Medicine, Kunshan, China
Yong Wang
Orthopedic Center, Kunshan Hospital of Traditional Chinese Medicine, Kunshan, China
Xiang Chen
Orthopedic Center, Kunshan Hospital of Traditional Chinese Medicine, Kunshan, China
Bin Chen
Orthopedic Center, Kunshan Hospital of Traditional Chinese Medicine, Kunshan, China
Yong Chen
Orthopedic Center, Kunshan Hospital of Traditional Chinese Medicine, Kunshan, China

ABSTRACT

The notorious lung metastatic capability of osteosarcoma aggravates patient mortality and remains the primary challenge to be overcome. We investigated the effect of (−)-epigallocatechin-3-gallate (EGCG) on the metastasis capability of osteosarcoma cells. We performed cytotoxicity assays (MTT) to determine the appropriate concentration of EGCG for experiments. Migration, invasion, wound-healing, and adhesion assays were performed to assess the effect of EGCG on the metastasis of osteosarcoma. Changes in the mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway were investigated using Western blot analyses. In addition, a MEK inhibitor (U0126) was used in invasion assays to determine the effect of the MEK/ERK signaling pathway. We found that EGCG may markedly inhibit the migration and invasion capacity of osteosarcoma cells, which occurred concurrently with inhibition of the expression of phospho-MEK and phospho-ERK. Inhibitors of MEK inhibited the invasion of osteosarcoma cells, and this effect could be enhanced by EGCG. We also detected the expression of c-Jun N-terminal kinase, p38, and their respective phospho-proteins, but did not find any meaningful changes. Taken together, our results demonstrated that EGCG could inhibit the metastasis capability of osteosarcoma cells by inhibiting MEK/ERK signaling activity and may provide new therapeutic value for osteosarcoma.