Lei Wang1, Yijun Qi2, Ying Xiong2, Zhiqiang Peng2, Qiang Ma2, Yue Zhang2, Jian Song1, Junfang Zheng3,4. 1. Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, P.R. China. 2. Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing, P.R. China. 3. Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing, P.R. China zhengjf@ccmu.edu.cn. 4. Beijing Key Laboratory for Tumor Invasion and Metastasis, Beijing International Cooperation Base for Science and Technology on China-UK Cancer Research, Beijing, P.R. China.
Abstract
BACKGROUND: Expression of ezrin-radixin-moesin-binding phosphoprotein-50 (EBP50) is correlated with human breast and cervical cancer development, but its effects on the metastasis of breast and cervical cancer and the underlying mechanism are not fully understood. MATERIALS AND METHODS: In this study, EBP50 was overexpressed in MDA-MB-231 breast cancer and HeLa cervical cancer cells; moreover, EBP50 was knocked-down in MCF-7 breast cancer cells and HeLa cells. Metastasis-related ability and matrix metalloproteinase-2 (MMP-2) activity of these cells were investigated. RESULTS: Cell adhesion, wound-healing and invasion were significantly suppressed in EBP50-overexpressing cells. Contrarily, EBP50-knockdown promoted cell adhesion, wound healing and invasion. EBP50 overexpression inhibited MMP-2 activity, and the knockdown of EBP50 promoted the activity of MMP-2, suggesting that EBP50 inhibited cell metastasis via suppression of MMP-2 activity. CONCLUSION: Our work reveals the anti-metastatic effect and a new mechanism of EBP50 action in breast and cervical cancer cells. Copyright
BACKGROUND: Expression of ezrin-radixin-moesin-binding phosphoprotein-50 (EBP50) is correlated with humanbreast and cervical cancer development, but its effects on the metastasis of breast and cervical cancer and the underlying mechanism are not fully understood. MATERIALS AND METHODS: In this study, EBP50 was overexpressed in MDA-MB-231 breast cancer and HeLa cervical cancer cells; moreover, EBP50 was knocked-down in MCF-7 breast cancer cells and HeLa cells. Metastasis-related ability and matrix metalloproteinase-2 (MMP-2) activity of these cells were investigated. RESULTS: Cell adhesion, wound-healing and invasion were significantly suppressed in EBP50-overexpressing cells. Contrarily, EBP50-knockdown promoted cell adhesion, wound healing and invasion. EBP50 overexpression inhibited MMP-2 activity, and the knockdown of EBP50 promoted the activity of MMP-2, suggesting that EBP50 inhibited cell metastasis via suppression of MMP-2 activity. CONCLUSION: Our work reveals the anti-metastatic effect and a new mechanism of EBP50 action in breast and cervical cancer cells. Copyright