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Silencing of AFAP1-AS1 lncRNA impairs cell proliferation and migration by epigenetically promoting DUSP5 expression
Shuai Zhang1, Yanfen Zou2, Xiaotong Tang3
1Department of Critical Care Medicine, The Second Hospital of Nanjing, Nanjing University of Chinese Medicine, Jiangsu Province, China.
Insights
Pre-eclampsia (PE) involves abnormal long noncoding RNA (lncRNA) expression. This study found lncRNA AFAP1-AS1 is downregulated in PE, impacting trophoblast cells and suggesting it as a potential biomarker and therapeutic target.
Area of Science:
- Obstetrics and Gynecology
- Molecular Biology
- Genetics
Background:
- Pre-eclampsia (PE) is a leading cause of maternal and perinatal mortality worldwide.
- Aberrant expression of long noncoding RNAs (lncRNAs) is implicated in PE pathogenesis.
- Understanding the role of specific lncRNAs in PE is crucial for developing diagnostic and therapeutic strategies.
Purpose of the Study:
- To investigate the role of lncRNA AFAP1-AS1 in the pathogenesis of pre-eclampsia.
- To elucidate the underlying molecular mechanism of AFAP1-AS1 in human trophoblast cells.
Main Methods:
- Quantitative analysis of AFAP1-AS1 expression in pre-eclamptic placentas.
- In vitro functional assays (e.g., knockdown studies) in human trophoblast cells.
- Investigation of molecular interactions involving AFAP1-AS1, EZH2, and DUSP5 promoter activity.
Main Results:
- lncRNA AFAP1-AS1 expression was significantly downregulated in pre-eclamptic placentas compared to normal placentas.
- Knockdown of AFAP1-AS1 in human trophoblast cells inhibited cell proliferation, migration, and invasion.
- AFAP1-AS1 was found to interact with EZH2, suppressing DUSP5 expression via H3K27m3 modification at the DUSP5 promoter.
Conclusions:
- lncRNA AFAP1-AS1 plays a critical role in regulating trophoblast cell function and is involved in pre-eclampsia pathogenesis.
- AFAP1-AS1 may serve as a potential prognostic biomarker for pre-eclampsia.
- Targeting AFAP1-AS1 presents a novel therapeutic strategy for pre-eclampsia.
Abstract:
As a unique and common obstetric complication of pregnant women, pre-eclampsia (PE) has been the first leading cause of maternal and perinatal morbidity and mortality in the world. Mounting studies have demonstrated that an abnormality of long noncoding RNA (lncRNA) expression was related to the pathological process of PE. Here, we showed that lncRNA AFAP1-AS1 was markedly downregulated in pre-eclamptic placentas. We further investigated the mechanism underlying the regulatory role of AFAP1-AS1 in PE using human trophoblast cells. In vitro functional assays revealed that AFAP1-AS1 knockdown inhibited trophoblast proliferation, migration, and invasion. Moreover, AFAP1-AS1 interacts with EZH2 and inhibits DUSP5 expression through modulating H3K27m3 in the DUSP5 promoter of trophoblast cells, thus being involved in PE pathogenesis. Overall, these findings suggest that AFAP1-AS1 could potentially become a prognostic biomarker as well as a new therapeutic target for PE.
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