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CircSTAM inhibits migration and invasion of trophoblast cells by regulating miR-148a-5p/PTEN axis

BACKGROUND: The mechanisms underlying the pathogenesis of preeclampsia (PE) remains unclear. Exploring the molecular players in PE progression can provide insights into targeted therapy. METHODS: The expression levels of circSTAM in placental chorionic tissues of PE patients and normal pregnant wome...

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Detalles Bibliográficos
Autores principales: Chen, Lingfeng, Yan, Jinyu, Zhang, Haiyan, Xu, Jia, Chen, Xiaopei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9840740/
https://www.ncbi.nlm.nih.gov/pubmed/36471201
http://dx.doi.org/10.1007/s10815-022-02660-4
Descripción
Sumario:BACKGROUND: The mechanisms underlying the pathogenesis of preeclampsia (PE) remains unclear. Exploring the molecular players in PE progression can provide insights into targeted therapy. METHODS: The expression levels of circSTAM in placental chorionic tissues of PE patients and normal pregnant women were compared by RT-qPCR. CircSTAM was knocked down by small interfering RNA to investigate its role in migration, invasion and epithelial-mesenchymal transformation (EMT) of trophoblast HTR-8/SVneo cells. The downstream target of circSTAM was predicted using online bioinformatics resources, and their molecular interaction was examined by luciferase reporter assay. RESULTS: CircSTAM was upregulated in PE placenta tissues in comparison to normal placental tissues. CircSTAM knockdown significantly enhanced cellular invasion, migration, as well as EMT. Mir-148a-5p was identified as a target of circSTAM to regulate cell migration and invasion. Mir-148a-5p negatively regulated PTEN expression in trophoblast HTR-8 /SVneo cells. CONCLUSION: In summary, circSTAM upregulation in PE trophoblasts promoted the invasion, migration and EMT. CircSTAM may modulate trophoblast phenotype by impinging on mir-148a-5p/PTEN axis. These data provided novel insights into the pathogenesis of PE.