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- Title
miR-342-3p suppresses cell migration and invasion in preeclampsia by targeting platelet-derived growth factor receptor α.
- Authors
Yang, Xiuhua; Guo, Feng
- Abstract
miR-342-3p expression was increased in the placentas of women with preeclampsia (PE) according to previous examinations; the mechanism underlying the development and progression of PE requires further investigation. The present study aimed to explore the mechanism and functionality of microRNA (miR)-342-3p in trophoblastic cells. The expression of miR-342-3p and platelet-derived growth factor receptor α (PDGFRA) in the placentas of 30 patients with PE and 30 normal controls was detected. In addition, HTR8/SVneo cells were transfected with miR-342-3p mimics, small interfering RNA (siR)-PDGFRA or their corresponding negative controls; then the proliferation, migration, invasion and the distribution of the cell cycle of these cells were analyzed. Additionally, a dual-luciferase reporter assay was performed. According to these analyses, the expression of miR-342-3p was significantly increased, while that of PDGFRA was significantly lower in the PE group compared with the normal group. Transfection with miR-342-3p mimics led to a significant decrease in cell proliferation, migration and invasion, and also affected the cell cycle. Furthermore, miR-342-3p mimics reduced the expression of PDGFRA; miR-342-3p overexpression also reduced the mRNA and protein levels of BCL-2 and Caspase-3. In addition, transfection of siR-PDGFRA exhibited similar effects to those of miR-342-3p mimics. Finally, PDGFRA was reported to be a direct target of miR-342-3p. In conclusion, miR-342-3p was proposed to inhibit the proliferation, migration, invasion and G1/S phase transition of HTR8/SVneo cells by suppressing PDGFRA. Our findings suggest that miR-342-3p may be a novel clinical indicator or prognostic marker for PE.
- Subjects
PLATELET-derived growth factor receptors; CIRCULAR RNA; CELL migration; SMALL interfering RNA; CELL cycle; PREECLAMPSIA; MICRORNA
- Publication
Molecular Medicine Reports, 2019, Vol 20, Issue 2, p1772
- ISSN
1791-2997
- Publication type
Article
- DOI
10.3892/mmr.2019.10372