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首页> 外文期刊>Journal of King Saud University >MicroRNA-26b-3p inhibits human trophoblast cell proliferation, invasion and resistance to apoptosis via targeting SHBG
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MicroRNA-26b-3p inhibits human trophoblast cell proliferation, invasion and resistance to apoptosis via targeting SHBG

机译：MicroRNA-26B-3P通过靶向SHB抑制人滋养细胞增殖，侵袭和对细胞凋亡的抗性

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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.
机译：异常升高的肾凋亡和滋养细胞侵袭的凋亡和功能障碍在预先兰克血症中发挥关键作用。但是，该机制仍然不清楚。我们的研究通过靶向性激素结合球蛋白（SHBG）来研究MicroRNA-26B-3P（miR-26b-3p）在滋养细胞生长中的作用。在本研究中使用人滋养细胞系HTR8-SVNEO。进行MiR-26B-3P和SHBG的增益和函数丧失，然后用CCK-8和EDU测定检测细胞活力。使用流式细胞术检测细胞凋亡，并用Transwell测定评估细胞侵袭和迁移。用RT-PCR和Western印迹分析测量MiR-26B-3P转染后SHBG，Caspase-3和Bcl-2的表达水平。通过生物信息预测分析MiR-26B-3P和SHBG的序列，并用双荧光素酶报告结果证实。发现MiR-26B-3P的过表达抑制了HTR8-Svneo细胞增殖，侵袭和迁移，同时增加了细胞凋亡和G0 / G1相处的细胞周期停滞。突变水平的miR-26b-3p降低了SHBG的表达。生物信息化预测和双荧光素酶测定鉴定了miR-26b-3p和htr8-svneo的关系。 SHBG的下调表现出与HTR8-Svneo细胞生长的效果类似于miR-26b-3p的过度表达。结论：miR-26b-3p靶向shbg并降低SHBG表达。它抑制人滋养细胞增殖，侵袭和滋养细胞死亡的侵袭。本研究提供了预口普拉姆的机制。性激素结合球蛋白：shbg; miR-26b-3p：microRNA-26B-3P; CCK-8：Cell-Counting Kit-8; RT-PCR：实时聚合酶链式反应; 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，带有吐温。

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