ArticleExperimental and therapeutic medicine2020
MicroRNA-27a inhibits trophoblast cell migration and invasion by targeting SMAD2: Potential role in preeclampsia.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Review
- Cell-free mitochondrial DNA and microRNA-137 for early diagnosis of preeclampsia.Frontiers in cardiovascular medicine · 2026Article
- miR-27a rs895819 Polymorphism and Recurrent Pregnancy Loss in Caucasian Women: A Novel Genetic Risk Factor in a Challenging Fertility Dilemma.Current issues in molecular biology · 2025Article
- Non-coding RNAs: the architects of placental development and pregnancy success.Molecular genetics and genomics : MGG · 2025Review
- Vascular Endothelial Growth Factor Receptor 2: Molecular Mechanism and Therapeutic Potential in Preeclampsia Comorbidity with Human Immunodeficiency Virus and Severe Acute Respiratory Syndrome Coronavirus 2 Infections.International journal of molecular sciences · 2022Review
- Micro-RNAs in Human Placenta: Tiny Molecules, Immense Power.Molecules (Basel, Switzerland) · 2022Review
- Article
- Increased FUN14 domain containing 1 (FUNDC1) ubiquitination level inhibits mitophagy and alleviates the injury in hypoxia-induced trophoblast cells.Bioengineered · 2022Article
- Preeclamptic Women Have Disrupted Placental microRNA Expression at the Time of Preeclampsia Diagnosis: Meta-Analysis.Frontiers in bioengineering and biotechnology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Preeclampsia (PE) is a severe idiopathic obstetric complication that occurs worldwide. Insufficient trophoblast invasion is a characteristic of the pathogenesis of PE. MicroRNA-27a (miR-27a) has been reported to be highly expressed in PE placentas. The aim of the present study was to investigate the role and underlying mechanisms of miR-27a in the pathogenesis of PE. The expression level of miR-27a was evaluated in the placenta and serum from patients with PE and healthy pregnant women. Cell Counting Kit-8 and flow cytometry assays were performed to detect human HTR-8/SVneo trophoblast proliferation and apoptosis after miR-27a overexpression or inhibition. In addition, Transwell assays were used to measure cell migration and invasion. A luciferase reporter assay was performed to determine the interaction between miR-27a and SMAD2. The present results suggested that miR-27a expression level was significantly increased in PE placentas and serum. In addition, miR-27a overexpression suppressed cell migratory and invasive abilities, impaired proliferation and promoted apoptosis in human trophoblasts. It was demonstrated that miR-27a may target SMAD and contribute to trophoblast invasion. Collectively, the results of the present study suggested that miR-27a inhibited trophoblast cell migration and invasion by targeting SMAD2, thus presenting a promising therapeutic target for PE.
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