دورية أكاديمية
Nuclear Factor-Kappa B-induced miRNA-518a-5p represses trophoblast cell migration and invasion by the Nuclear Factor-Kappa B pathway
العنوان: | Nuclear Factor-Kappa B-induced miRNA-518a-5p represses trophoblast cell migration and invasion by the Nuclear Factor-Kappa B pathway |
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المؤلفون: | XING PENG, RUIRUI ZHANG, YUMEI ZHANG, CHUNYAN CAI |
المصدر: | Anais da Academia Brasileira de Ciências, Vol 95, Iss 1 (2023) |
بيانات النشر: | Academia Brasileira de Ciências, 2023. |
سنة النشر: | 2023 |
المجموعة: | LCC:Science |
مصطلحات موضوعية: | preeclampsia, HTR8/SVneo, invasion, NF-κB transcriptional factor, miR-518a-5p, Science |
الوصف: | Abstract Preeclampsia is associated with the insufficient invasion of trophoblasts. NF-κB is a transcription factor in almost all mammalian cells and has been validated to be upregulated in the maternal circulation and placenta of women with preeclampsia. MiR-518a-5p is also overexpressed in pre-eclamptic placenta. The present study was designed to explore whether NF-κB can transcriptionally activate miR-518a-5p and investigate the influences of miR-518a-5p on the viability, apoptosis, migration, and invasion of HTR8/SVneo trophoblast. In situ hybridization and real time polymerase chain reaction were used to reveal miR-518a-5p expression in placenta tissues and HTR8/SVneo cells, respectively. Cell migration and invasion were detected using Transwell inserts. Our findings indicated that NF-κB p52, p50, and p65 can bind to miR-518a-5p gene promoter. MiR-518a-5p further influences the levels of p50 and p65 but not p52. HTR8/SVneo cell viability and apoptosis were not influenced by miR-518a-5p. However, miR-518a-5p represses the migratory/invasive capacities of HTR8/SVneo cell and decreased gelatinolytic activity of MMP2 and MMP9, which was reversed by an NF-κB inhibitor. To sum up, miR-518a-5p is induced by NF-κB and represses trophoblast cell migration and invasion by the NF-κB pathway. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 1678-2690 0001-3765 |
Relation: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652023000100804&lng=en&tlng=en; http://www.scielo.br/pdf/aabc/v95n1/0001-3765-aabc-95-01-e20220596.pdf; https://doaj.org/toc/1678-2690 |
DOI: | 10.1590/0001-3765202320220596 |
URL الوصول: | https://doaj.org/article/d4b46a3d825645cdabf813a1ea7f6b49 |
رقم الأكسشن: | edsdoj.4b46a3d825645cdabf813a1ea7f6b49 |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 16782690 00013765 |
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DOI: | 10.1590/0001-3765202320220596 |