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LINC01541 overexpression attenuates the 17β-Estradiol-induced migration and invasion capabilities of endometrial stromal cells.
Systems Biology in Reproductive Medicine ( IF 2.1 ) Pub Date : 2019-01-04 , DOI: 10.1080/19396368.2018.1549290
Hong Mai 1 , Yeping Wei 1 , Yan Yin 1 , Shijin Huang 1 , Huisi Lin 2 , Yan Liao 1 , Xupeng Liu 1 , Xianfeng Chen 1 , Haijuan Shi 1 , Chuanzhong Liu 1 , Hong Xu 2
Affiliation  

Endometriosis affects 6–10% of healthy women of reproductive age. Therefore, it is important to study the molecular mechanism by which endometriosis develops. This study examined whether aberrant expression of LINC01541 contributes to the pathogenesis of endometriosis. Human endometrial stromal cells (ESCs) were stimulated with 10 nmol/L of 17β-Estradiol (17β-E2) to simulate ectopic cells found in endometriosis. Next, the levels of proteins related to the epithelial-mesenchymal transition (EMT), cell invasion, and metastasis were investigated. The effects of LINCO1541 silencing and overexpression were also examined in ESCs. Cell proliferation and apoptosis were detected by cell counting kit-8 and flow cytometry assays, respectively. ESCs stimulated with 17β-E2 displayed increased levels of N-Cadherin and vimentin expression, but decreased levels of E-Cadherin expression. 17β-E2 promoted the migration and invasion of ESCs, and those affects were partially reversed by overexpression of LINC01541. Furthermore, silencing of LINC01541 attenuated apoptosis and promoted the EMT of ESCs, while overexpression of LINC01541 stimulated cell apoptosis, increased the levels of caspase 3 protein, and decreased the levels of B cell leukemia/lymphoma 2 protein. Overexpression of LINC01541 also decreased the expression of vascular endothelial growth factor A (VEGFA) by repressing the Wnt/β-catenin pathway. Our, results suggest that LINC01541 can inhibit the EMT process, metastasis of ESCs, and VEGFA expression by regulating the Wnt/β-catenin pathway, which may play an important role in the pathogenesis of endometriosis.

Abbreviations: ESCs: endometrial stromal cells; 17β-E2: 17β-Estradiol; EMT: epithelial-mesenchymal transition; CASP3: caspase 3; BCL2: B cell leukemia/lymphoma 2; VEGFA: vascular endothelial growth factor A; lncRNA: long non-coding RNA; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; RT-qPCR: reverse transcription-quantitative polymerase chain reaction



中文翻译:

LINC01541过表达减弱了17β-雌二醇诱导的子宫内膜基质细胞的迁移和侵袭能力。

子宫内膜异位症影响6-10%的生殖年龄健康女性。因此,重要的是研究子宫内膜异位症发展的分子机制。这项研究检查了LINC01541的异常表达是否有助于子宫内膜异位症的发病机理。用10 nmol / L的17β-雌二醇(17β-E2)刺激人子宫内膜基质细胞(ESC),以模拟子宫内膜异位症中发现的异位细胞。接下来,研究了与上皮-间质转化(EMT),细胞侵袭和转移相关的蛋白质水平。在ESC中还检查了LINCO1541沉默和过表达的影响。通过细胞计数试剂盒8和流式细胞仪分别检测细胞增殖和凋亡。用17β-E2刺激的ESC的N-钙黏着蛋白和波形蛋白表达水平增加,但E-钙黏着蛋白表达水平下降。17β-E2促进了ESC的迁移和侵袭,这些影响被LINC01541的过表达部分逆转。此外,LINC01541的沉默可减弱细胞凋亡并促进ESC的EMT,而LINC01541的过表达则刺激细胞凋亡,增加caspase 3蛋白的水平,并降低B细胞白血病/淋巴瘤2蛋白的水平。LINC01541的过表达还通过抑制Wnt /β-catenin途径而降低了血管内皮生长因子A(VEGFA)的表达。我们的研究结果表明,LINC01541可通过调节Wnt /β-catenin途径来抑制EMT过程,ESC的转移和VEGFA的表达,这可能在子宫内膜异位症的发病机制中起重要作用。17β-E2促进了ESC的迁移和侵袭,这些影响被LINC01541的过表达部分逆转。此外,LINC01541的沉默可减弱细胞凋亡并促进ESC的EMT,而LINC01541的过表达则刺激细胞凋亡,增加caspase 3蛋白的水平,并降低B细胞白血病/淋巴瘤2蛋白的水平。LINC01541的过表达还通过抑制Wnt /β-catenin途径而降低了血管内皮生长因子A(VEGFA)的表达。我们的研究结果表明,LINC01541可通过调节Wnt /β-catenin途径来抑制EMT过程,ESC的转移和VEGFA的表达,这可能在子宫内膜异位症的发病机制中起重要作用。17β-E2促进了ESC的迁移和侵袭,这些影响被LINC01541的过表达部分逆转。此外,LINC01541的沉默可减弱细胞凋亡并促进ESC的EMT,而LINC01541的过表达则刺激细胞凋亡,增加caspase 3蛋白的水平,并降低B细胞白血病/淋巴瘤2蛋白的水平。LINC01541的过表达还通过抑制Wnt /β-catenin途径而降低了血管内皮生长因子A(VEGFA)的表达。我们的研究结果表明,LINC01541可通过调节Wnt /β-catenin途径来抑制EMT过程,ESC的转移和VEGFA的表达,这可能在子宫内膜异位症的发病机制中起重要作用。LINC01541的沉默可减弱细胞凋亡并促进ESC的EMT,而LINC01541的过表达则刺激细胞凋亡,增加caspase 3蛋白水平并降低B细胞白血病/淋巴瘤2蛋白水平。LINC01541的过表达还通过抑制Wnt /β-catenin途径而降低了血管内皮生长因子A(VEGFA)的表达。我们的研究结果表明,LINC01541可通过调节Wnt /β-catenin途径来抑制EMT过程,ESC的转移和VEGFA的表达,这可能在子宫内膜异位症的发病机制中起重要作用。LINC01541的沉默可减弱细胞凋亡并促进ESC的EMT,而LINC01541的过表达则刺激细胞凋亡,增加caspase 3蛋白水平并降低B细胞白血病/淋巴瘤2蛋白水平。LINC01541的过表达还通过抑制Wnt /β-catenin途径而降低了血管内皮生长因子A(VEGFA)的表达。我们的结果表明,LINC01541可通过调节Wnt /β-catenin途径来抑制EMT过程,ESC的转移和VEGFA的表达,这可能在子宫内膜异位症的发病机理中起重要作用。LINC01541的过表达还通过抑制Wnt /β-catenin途径而降低了血管内皮生长因子A(VEGFA)的表达。我们的研究结果表明,LINC01541可通过调节Wnt /β-catenin途径来抑制EMT过程,ESC的转移和VEGFA的表达,这可能在子宫内膜异位症的发病机制中起重要作用。LINC01541的过表达还通过抑制Wnt /β-catenin途径而降低了血管内皮生长因子A(VEGFA)的表达。我们的研究结果表明,LINC01541可通过调节Wnt /β-catenin途径来抑制EMT过程,ESC的转移和VEGFA的表达,这可能在子宫内膜异位症的发病机制中起重要作用。

缩写: ESCs:子宫内膜基质细胞;17β-E2:17β-雌二醇;EMT:上皮-间质转化;CASP3:胱天蛋白酶3;BCL2:B细胞白血病/淋巴瘤2;VEGFA:血管内皮生长因子A;lncRNA:长的非编码RNA;GAPDH:3-磷酸甘油醛脱氢酶;RT-qPCR:逆转录定量聚合酶链反应

更新日期:2019-01-04
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