Wang Lei, Qi Yijun, Xiong Ying, Peng Zhiqiang, Ma Qiang, Zhang Yue, Song Jian, Zheng Junfang
Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, P.R. China.
Department of Biochemistry and Molecular Biology, Capital Medical University, Beijing, P.R. China.
Anticancer Res. 2017 Aug;37(8):4353-4360. doi: 10.21873/anticanres.11829.
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.
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.
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.
Our work reveals the anti-metastatic effect and a new mechanism of EBP50 action in breast and cervical cancer cells.
埃兹蛋白-根蛋白-膜突蛋白结合磷蛋白50（EBP50）的表达与人类乳腺癌和宫颈癌的发展相关，但其对乳腺癌和宫颈癌转移的影响及潜在机制尚未完全明确。
在本研究中，EBP50在MDA-MB-231乳腺癌细胞和HeLa宫颈癌细胞中过表达；此外，EBP50在MCF-7乳腺癌细胞和HeLa细胞中被敲低。研究了这些细胞的转移相关能力和基质金属蛋白酶-2（MMP-2）活性。
EBP50过表达的细胞中，细胞黏附、伤口愈合和侵袭能力均显著受到抑制。相反，EBP50敲低促进了细胞黏附、伤口愈合和侵袭。EBP50过表达抑制了MMP-2活性，而EBP50敲低则促进了MMP-2的活性，这表明EBP50通过抑制MMP-2活性来抑制细胞转移。
我们的研究揭示了EBP50在乳腺癌和宫颈癌细胞中的抗转移作用及新的作用机制。
