Smad4 mediates malignant behaviors of human ovarian carcinoma cell through the effect on expressions of E-cadherin, plasminogen activator inhibitor-1 and VEGF

作者：Chen Chen, Ming‐Zhong Sun, Shuqing Liu, Dongmei Yeh, Lijun Yu, Yang Song, Lin-Lin Gong, Lihong Hao, Jun Hu, Shu-Juan Shao · 发表于：BMB Reports · 年份：2010 · DOI：10.5483/bmbrep.2010.43.8.554 · 被引用次数：22 · 研究领域：TGF-β signaling in diseases、Pancreatic and Hepatic Oncology Research、Cancer-related gene regulation

Smad4 is involved in cancer progression and metastasis. Using a pair of human syngeneic epithelial ovarian cancer cells with low (HO-8910) and high (HO-8910PM) metastatic abilities, we aimed to reveal the role of Smad4 in ovarian cancer metastasis in vitro. Smad4 was down-regulated in HO-8910PM cell line relative to HO-8910 by implicating Smad4 was probably a potential tumor suppressor gene for ovarian cancer. Re-expression of Smad4 decreased the migration ability and inhibited the invasion capacity of HO-8910PM, while promoted the cell adhesion capacity for HO-8910PM. The stable expression of Smad4 increased the expression of E-cadherin, reduced the expression of plasminogen activator inhibitor-1 (PAI-1) and slightly down-regulated the expression of VEGF. Smad4 suppresses human ovarian cancer cell metastasis potential through its effect on the expressions of PAI-1, E-cadherin and VEGF. Results from current work implicate Smad4 might suppress the invasion and metastasis of human ovarian tumor cells through a TGF-Beta/Smad-mediated pathway.