Aberrant increased apoptosis and dysfunction in migration and invasion of trophoblast cell play key role in preeclampsia. However, the mechanism remains unclear. Our study investigated the roles of microRNA-26b-3p (miR-26b-3p) in trophoblast cell growth by targeting sex hormone binding globulin (SHBG). Human trophoblast cell line HTR8-SVneo was used in this study. Gain- and loss-of-functions of miR-26b-3p and SHBG were performed, and then the cell viability was detected with CCK-8 and EdU assays. Cell apoptosis was detected using flow cytometry, and the cell invasion and migration were evaluated with transwell assays. The expression level of SHBG, caspase-3 and Bcl-2 after miR-26b-3p transfection was measured with RT-PCR and western blot analysis. Matching the sequence of miR-26b-3p and SHBG was analyzed through bioinformatic prediction and confirmed with dual luciferase reporter assay. It is found that overexpression of miR-26b-3p inhibited HTR8-SVneo cell proliferation, invasion and migration, while increased cell apoptosis and induced cell cycle arrest at the G0/G1 phase. Elvated level of miR-26b-3p decreased the expression of SHBG. Bioinformatic prediction and dual luciferase assay identified the relation of miR-26b-3p and HTR8-SVneo. Downregulation of SHBG exhibited similar effects on HTR8-SVneo cell growth with overexpression of miR-26b-3p. Conclusion: MiR-26b-3p targets SHBG and decreases SHBG expression. It inhibits human trophoblast cell proliferation, invasion and resistance to death of trophoblast cell. This study provided a mechanism for preeclampsia. Sex hormone binding globulin: SHBG; miR-26b-3p: microRNA-26b-3p; CCK-8: Cell-Counting Kit-8; RT-PCR: Real time polymerase chain reaction; NC: miR-26b-3p mimic negative control or SHBG negative control siRNA; inhibitor NC: negative control inhibitor; TBST: Tris-buffered saline with Tween.

异常增加的细胞凋亡和滋养细胞迁移和侵袭功能障碍在先兆子痫中起关键作用。但是，机制尚不清楚。我们的研究通过靶向性激素结合球蛋白（SHBG）研究了microRNA-26b-3p（miR-26b-3p）在滋养细胞生长中的作用。在该研究中使用了人类滋养细胞细胞系HTR8-SVneo。进行miR-26b-3p和SHBG的功能获得和丧失，然后通过CCK-8和EdU分析检测细胞活力。使用流式细胞仪检测细胞凋亡，并通过transwell分析评估细胞的侵袭和迁移。通过RT-PCR和western blot分析检测miR-26b-3p转染后SHBG，caspase-3和Bcl-2的表达水平。通过生物信息学预测分析miR-26b-3p和SHBG的匹配序列，并通过双重荧光素酶报告基因检测法进行确认。发现miR-26b-3p的过表达抑制HTR8-SVneo细胞的增殖，侵袭和迁移，同时增加细胞凋亡并诱导细胞周期停滞在G0 / G1期。升高水平的miR-26b-3p降低了SHBG的表达。生物信息学预测和双重荧光素酶测定确定了miR-26b-3p和HTR8-SVneo的关系。SHBG的下调与miR-26b-3p的过表达对HTR8-SVneo细胞的生长表现出相似的影响。升高水平的miR-26b-3p降低了SHBG的表达。生物信息学预测和双重荧光素酶测定确定了miR-26b-3p和HTR8-SVneo的关系。SHBG的下调与miR-26b-3p的过表达对HTR8-SVneo细胞的生长表现出相似的影响。升高水平的miR-26b-3p降低了SHBG的表达。生物信息学预测和双重荧光素酶测定确定了miR-26b-3p和HTR8-SVneo的关系。SHBG的下调与miR-26b-3p的过表达对HTR8-SVneo细胞的生长表现出相似的影响。结论： MiR-26b-3p靶向SHBG并降低SHBG表达。它抑制人滋养层细胞的增殖，侵袭和对滋养层细胞死亡的抵抗。该研究提供了先兆子痫的机制。性激素结合球蛋白：SHBG；miR-26b-3p：microRNA-26b-3p；CCK-8：细胞计数试剂盒8；RT-PCR：实时聚合酶链反应；NC：miR-26b-3p模拟阴性对照或SHBG阴性对照siRNA；抑制剂NC：阴性对照抑制剂；TBST：Tris缓冲盐水和Tween。