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Updated: Aug 26, 2025

Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library
Published on: April 6, 2012
Downregulation of Circ_0088196 Contributes to the Development of Trophoblastic Cells through miR-133b Sponging
Yubo Shi1, Lianxiao Zhang1, Linlin Wang1
1Department of Obstetric, Ningbo First Hospital, Ningbo, China.
Insights
Circular RNA hsa_circ_0088196 promotes preeclampsia progression by regulating miR-133b and AHNAK. Knockdown of circ_0088196 enhances trophoblastic cell development, suggesting a therapeutic target for preeclampsia.
Area of Science:
- Molecular Biology
- Reproductive Medicine
- Genetics
Background:
- Preeclampsia (PE) is a common gestational disease.
- Circular RNAs (circRNAs) are implicated in various diseases.
- Hsa_circ_0088196 (circ_0088196) is upregulated in PE tissues.
Purpose of the Study:
- To investigate the role of circ_0088196 in preeclampsia.
- To explore the molecular mechanisms underlying circ_0088196 function in trophoblastic cells.
Main Methods:
- RT-qPCR to quantify circ_0088196, miR-133b, and AHNAK levels.
- Cell proliferation, cycle, apoptosis, migration, and invasion assays.
- Dual-luciferase reporter and RNA pull-down assays to confirm interactions.
Main Results:
- Circ_0088196 was upregulated in PE patients.
- Knockdown of circ_0088196 promoted trophoblastic cell proliferation, cell cycle, migration, and invasion.
- Circ_0088196 acts as a sponge for miR-133b, regulating AHNAK expression.
Conclusions:
- Circ_0088196 knockdown facilitates trophoblastic cell development.
- The circ_0088196/miR-133b/AHNAK axis plays a crucial role in PE progression.
- Further in vivo studies are needed to validate findings.
Objective:
Preeclampsia (PE) is the most common gestational disease related to various biomolecules, including circular RNA. Hsa_circ_0088196 (circ_0088196) was aberrantly upregulated in PE tissues.
Design:
This study focused on the further exploration of circ_0088196 in PE.
Methods:
Circ_0088196, microRNA-133b (miR-133b), and AHNAK Nucleoprotein (AHNAK) levels were examined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). EDU assay was used for proliferation detection. Cell cycle and apoptosis were analyzed using flow cytometry. Wound healing assay and transwell assay were performed to assess migration and invasion. The protein levels were determined via Western blot. Target analysis was conducted through dual-luciferase reporter assay and RNA pull-down assay.
Results:
Circ_0088196 upregulation was detected in PE patients. The knockdown of circ_0088196 induced the promotion of proliferation, cell cycle, migration, and invasion but not the inhibition of apoptosis in trophoblastic cells. Then, circ_0088196 was found to act as a sponge of miR-133b in HTR-8/SVneo cells. The inhibition of miR-133b abolished the regulation of si-circ_0088196 in trophoblastic cells. In addition, miR-133b targeted AHNAK and circ_0088196 evoked the expression change of AHNAK by sponging miR-133b. The function of circ_0088196 was also achieved by regulating AHNAK in trophoblastic cells.
Limitations:
The role of circ_0088196 in PE was not verified by in vivo experiments.
Conclusion:
The current evidence demonstrated that circ_0088196 knockdown facilitated trophoblastic cell development by regulating the levels of miR-133b and AHNAK, suggesting that circ_0088196 promoted the PE progression via the miR-133b/AHNAK axis.
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