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Expression of Talin-1 in endometriosis and its possible role in pathogenesis

机译:阴茎1在子宫内膜异位症中的表达及其在发病机制中可能的作用

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Endometriosis is a disease that involves active cell invasion and migration. Talin-1 can promote cell invasion, migration and adhension in various cancer cells, but its role in endometriosis has not been investigated. This study was to investigate the expression level of Talin-1 in endometriosis and the role of Talin-1 in the proliferation, adhesion, migration, and invasion of human endometrial stromal cells (ESCs). Ectopic and eutopic endometrial tissues were collected from women with endometriosis, and the control endometrial tissues were obtained from patients without endometriosis. The expression level of Talin-1 was detected in each sample using quantitative real-time polymerase chain reaction and immunohistochemistry. The expression of Talin-1 was inhibited using RNA interference in ESCs, and its proliferation, apoptosis, adhesion, migration, and invasion capacity were analyzed. Western blotting was performed to detect the expression of related molecules after the downregulation of Talin-1. The results showed that the mRNA and protein expression of Talin-1 were significantly increased in the ectopic endometrium and eutopic endometrial tissues compared with the controls. The knockdown of Talin-1 did not affect the proliferation and apoptosis of ESCs. The results indicated that the downexpression of Talin-1 inhibited the adhesion, invasion, and migration of ESCs. In addition, the expressions of N-cadherin, MMP-2, and integrin β3 were significantly lower after the deregulation of Talin-1, whereas the levels of E-cadherin were significantly increased. The expression of Talin-1 was increased in the ectopic and eutopic endometrial tissues compared with the control endometrium. The downregulation of Talin-1 inhibited the adhesion, invasion, and migration of ESCs.
机译:子宫内膜异位症是一种涉及活性细胞入侵和迁移的疾病。 Talin-1可以在各种癌细胞中促进细胞侵袭,迁移和腺体,但其在子宫内膜异位中的作用尚未得到调查。本研究是研究子宫内膜异位症中的瞳孔-1的表达水平以及倒下瞳-1在人子宫内膜基质细胞(ESC)的增殖,粘附,迁移和侵袭中的作用。从患有子宫内膜异位症的妇女收集异位和子宫子宫内膜组织,并从没有子宫内膜异位症的患者获得对照子宫内膜组织。使用定量的实时聚合酶链反应和免疫组化,在每个样品中检测到倒闭物1的表达水平。使用ESC的RNA干扰抑制了倒下的表达,并分析了其增殖,凋亡,粘附,迁移和侵袭能力。进行蛋白质印迹以检测瞳孔-1的下调后相关分子的表达。结果表明,与对照相比,异位子宫内膜和子宫内膜组织中,瞳孔-1的mRNA和蛋白表达显着增加。 Talin-1的敲低并不影响Escs的增殖和凋亡。结果表明,瞳孔-1的下抑制抑制了ESC的粘附,侵袭和迁移。另外,在倒下放松沉重后,N-Cadherin,MMP-2和整合蛋白β3的表达显着降低,而E-Cadherin的水平显着增加。与对照子宫内膜相比,异位和抑制子宫内膜组织中倒闭物-1的表达增加。瞳孔-1的下调抑制了ESC的粘附,侵袭和迁移。

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