PURPOSE Endometriosis is one of the most common, difficult, and complicated gynecological disorders. Vascular cell adhesion molecule 1 (VCAM-1) has been reported to be aberrantly expressed in patients with endometriosis. However, the exact role and mechanism of VCAM-1 in endometriosis remains unclear. METHODS The expression of transforming growth factor beta 1 (TGF-β1) and VCAM-1 was determined by quantitative real-time polymerase chain reaction and western blotting. Human endometriotic cells were cultured and their responsiveness to TGF-β1 was evaluated by Cell Counting Kit-8, 5-ethynyl-2'-deoxyuridine, and transwell migration and invasion assays. RESULTS The levels of TGF-β1 and VCAM-1 mRNA were upregulated in the endometriotic tissues. Knockdown of TGF-β1 in endometriotic cyst stromal cells caused a marked inhibition of cell proliferation, migration, and invasion. Treatment of endometriotic cyst stromal cells with TGF-β1 resulted in an obvious promotion of cell proliferation, migration, and invasion, and strikingly increased the protein expression of VCAM-1. Silencing of Smad3 abated TGF-β1-stimulated VCAM-1 expression. Furthermore, the promoting effects of TGF-β1 on the proliferation, migration, and invasion of endometriotic cyst stromal cells were blocked by silencing of VCAM-1. CONCLUSION Knockdown of VCAM-1 impedes TGF-β1-mediated proliferation, migration, and invasion of endometrial cells, thereby indicating that VCAM-1 may serve as a therapeutic target for endometriosis.

中文翻译：

---

击倒的血管细胞粘附分子1阻碍了转化生长因子β1介导的子宫内膜异位囊肿基质细胞的增殖，迁移和侵袭。

目的子宫内膜异位症是最常见，最困难和最复杂的妇科疾病之一。据报道，子宫内膜异位症患者异常表达了血管细胞粘附分子1（VCAM-1）。但是，尚不清楚VCAM-1在子宫内膜异位症中的确切作用和机制。方法采用定量实时聚合酶链反应和western blotting方法检测转化生长因子β1（TGF-β1）和VCAM-1的表达。培养人子宫内膜异位细胞，并通过Cell Counting Kit-8、5-乙炔基-2'-脱氧尿苷以及transwell迁移和侵袭试验评估其对TGF-β1的反应性。结果子宫内膜异位组织中TGF-β1和VCAM-1 mRNA的表达上调。子宫内膜异位囊肿基质细胞中TGF-β1的抑制导致细胞增殖的明显抑制，迁移和入侵。用TGF-β1处理子宫内膜异位囊肿基质细胞可明显促进细胞增殖，迁移和侵袭，并显着增加VCAM-1的蛋白表达。沉默Smad3减轻了TGF-β1刺激的VCAM-1表达。此外，通过使VCAM-1沉默，阻断了TGF-β1对子宫内膜异位囊肿基质细胞增殖，迁移和侵袭的促进作用。结论抑制VCAM-1可以阻止TGF-β1介导的子宫内膜细胞的增殖，迁移和侵袭，从而表明VCAM-1可以作为子宫内膜异位症的治疗靶点。并显着增加了VCAM-1的蛋白表达。沉默Smad3减轻了TGF-β1刺激的VCAM-1表达。此外，通过使VCAM-1沉默，阻断了TGF-β1对子宫内膜异位囊肿基质细胞增殖，迁移和侵袭的促进作用。结论抑制VCAM-1可以阻止TGF-β1介导的子宫内膜细胞的增殖，迁移和侵袭，从而表明VCAM-1可以作为子宫内膜异位症的治疗靶点。并显着增加了VCAM-1的蛋白表达。沉默Smad3减轻了TGF-β1刺激的VCAM-1表达。此外，通过使VCAM-1沉默，阻断了TGF-β1对子宫内膜异位囊肿基质细胞增殖，迁移和侵袭的促进作用。结论抑制VCAM-1可以阻止TGF-β1介导的子宫内膜细胞的增殖，迁移和侵袭，从而表明VCAM-1可以作为子宫内膜异位症的治疗靶点。