التفاصيل البيبلوغرافية
| العنوان: |
METTL3-mediated lncRNA HOXD-AS1 stability regulates inflammation, and the migration and invasion of trophoblast cells via the miR-135a/ β-TRCP axis |
| المؤلفون: |
Ling Wang, Li Shi, Bo Zhou, Lan Hong, Humin Gong, Dongcai Wu |
| المصدر: |
Non-coding RNA Research, Vol 9, Iss 1, Pp 12-23 (2024) |
| بيانات النشر: |
KeAi Communications Co., Ltd., 2024. |
| سنة النشر: |
2024 |
| المجموعة: |
LCC:Genetics |
| مصطلحات موضوعية: |
Preeclampsia, m6A methylation, lncRNA, Ubiquitin, Trophoblast, Genetics, QH426-470 |
| الوصف: |
Background: Preeclampsia (PE) is a serious pregnancy-specific syndrome associated with the inadequate invasion of trophoblast cells and inflammation of the uterus. A previous study found that lncRNA HOXD-AS1 promotes PE. However, its regulatory network requires additional exploration. Methods: HOXD-AS1-targeted miRNAs and genes were predicted by different databases in a bioinformatics analysis. The expression HOXD-AS1 and its potential m6A methylase (METTL3) were detected in placentas from healthy female patients with PE. The targeting relationship and role of the HOXD-AS1/miR-135a/β-TRCP axis in trophoblast cells were demonstrated by overexpression/knockdown assays. The levels of β-TRCP downstream pathway proteins IκBα, NF-κB, and p65 were measured. The levels of inflammatory factors in cell supernatants were detected by ELISA. To verify the molecular mechanism of β-TRCP in PE, IκBα was co-overexpressed in β-TRCP in trophoblast cells. Results: The levels of METTL3, HOXD-AS1, and β-TRCP were elevated in PE placental tissues, while miR-135a levels were reduced. MiR-135a was found to be targeted by HOXD-AS1, and HOXD-AS1 expression was maintained at a high level by METTL3-mediated m6A methylation. Overexpression of METTL3, HOXD-AS1, and β-TRCP, and knockdown of miR-135a in HTR-8/SVneo cells all inhibited cell invasion and migration, and promoted apoptosis and the secretion of inflammatory factors. Knockdown of METTL3, HOXD-AS1, and β-TRCP, and overexpression of miR-135a had the opposite effects. Furthermore, IκBα expression was negatively associated with β-TRCP expression, and the levels of NF-κB, p65, and NLRP3 were positively regulated by β-TRCP. A high level of β-TRCP expression attenuated the effect of HOXD-AS1 knockdown in trophoblast cells. Conclusion: METTL3 functioned to maintain a high level of HOXD-AS1 expression in PE, which influenced inflammation and the migration and invasion of trophoblast cells via the miR-135a/β-TRCP axis and NF-κB pathway. |
| نوع الوثيقة: |
article |
| وصف الملف: |
electronic resource |
| اللغة: |
English |
| تدمد: |
2468-0540 |
| Relation: |
http://www.sciencedirect.com/science/article/pii/S2468054023000793; https://doaj.org/toc/2468-0540 |
| DOI: |
10.1016/j.ncrna.2023.11.006 |
| URL الوصول: |
https://doaj.org/article/9ad7bc5482f4455695d3cc31ce2cff98 |
| رقم الانضمام: |
edsdoj.9ad7bc5482f4455695d3cc31ce2cff98 |
| قاعدة البيانات: |
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