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首页> 外文期刊>Cell death & disease. >miR-181a-5p suppresses invasion and migration of HTR-8/SVneo cells by directly targeting IGF2BP2
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miR-181a-5p suppresses invasion and migration of HTR-8/SVneo cells by directly targeting IGF2BP2

机译:miR-181a-5p通过直接靶向IGF2BP2抑制HTR-8 / SVneo细胞的侵袭和迁移

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Pre-eclampsia is a pregnancy-related disease that may cause maternal, neonatal and fetal morbidity and mortality and exists in 3–5% of pregnancies worldwide. The discovery of dysregulated microRNAs and their roles in placental development has provided a new avenue for elucidating the mechanism involved in this pregnancy-specific disorder. Here, the roles of human miR-181a-5p, a microRNA that is increased in both the plasma and placenta of severe pre-eclamptic patients, in invasion and migration of trophoblasts were investigated. Ectopic-expression of miR-181a-5p impaired the invasion and migration of HTR-8/SVneo cells, whereas miR-181a-5p inhibition had the opposite effects. IGF2BP2, which harbors a highly conserved miR-181a-5p-binding site within its 3?-UTR, was identified to be directly inhibited by miR-181a-5p. Moreover, siRNAs targeting IGF2BP2 imitated the effects of overexpressed miR-181a-5p on HTR-8/SVneo cell invasion and migration, whereas restoring IGF2BP2 expression by overexpressing a plasmid encoding IGF2BP2 partially reversed the studied inhibitory functions of miR-181a-5p. Thus, we demonstrated here that miR-181a-5p suppresses the invasion and migration of cytotrophoblasts, and its inhibitory effects were at least partially mediated by the suppression of IGF2BP2 expression, thus shedding new light on the roles of miR-181a-5p in the pathogenesis of severe pre-eclampsia.
机译:子痫前期是一种与妊娠有关的疾病,可能引起孕产妇,新生儿和胎儿的发病率和死亡率,并且在全球3%至5%的妊娠中都存在。失调的microRNA及其在胎盘发育中的作用的发现为阐明这种妊娠特异性疾病的机制提供了新途径。在这里,研究了人类miR-181a-5p(一种在严重先兆子痫患者的血浆和胎盘中均增加的微小RNA)在滋养细胞侵袭和迁移中的作用。 miR-181a-5p的异位表达损害了HTR-8 / SVneo细胞的侵袭和迁移,而miR-181a-5p的抑制作用却相反。 IGF2BP2在其3′-UTR中具有高度保守的miR-181a-5p结合位点,经鉴定被miR-181a-5p直接抑制。此外,靶向IGF2BP2的siRNA模仿了过表达的miR-181a-5p对HTR-8 / SVneo细胞侵袭和迁移的作用,而通过过表达编码IGF2BP2的质粒来恢复IGF2BP2的表达则部分逆转了miR-181a-5p的抑制功能。因此,我们在这里证明了miR-181a-5p抑制了细胞滋养细胞的侵袭和迁移,并且其抑制作用至少部分地受到了IGF2BP2表达的抑制,从而为miR-181a-5p在细胞凋亡中的作用提供了新的思路。重子痫前期的发病机理。

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