Key Laboratory for Proteomics of Liaoning Province, Dalian Medical University, Dalian 116044, China.
BMB Rep. 2010 Aug;43(8):554-60. doi: 10.5483/bmbrep.2010.43.8.554.
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.
Smad4 参与癌症的进展和转移。使用一对具有低(HO-8910)和高(HO-8910PM)转移能力的人同源上皮性卵巢癌细胞,我们旨在揭示 Smad4 在体外卵巢癌转移中的作用。Smad4 在 HO-8910PM 细胞系中的表达下调相对于 HO-8910,暗示 Smad4 可能是卵巢癌的潜在肿瘤抑制基因。Smad4 的重新表达降低了 HO-8910PM 的迁移能力并抑制了其侵袭能力,同时促进了 HO-8910PM 的细胞黏附能力。Smad4 的稳定表达增加了 E-钙黏蛋白的表达,降低了纤溶酶原激活物抑制剂-1(PAI-1)的表达,并略微下调了 VEGF 的表达。Smad4 通过对 PAI-1、E-钙黏蛋白和 VEGF 的表达的影响抑制人卵巢癌细胞的转移潜能。目前的工作结果表明,Smad4 可能通过 TGF-β/Smad 介导的途径抑制人卵巢肿瘤细胞的侵袭和转移。