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Long noncoding RNAs (lncRNAs) have been reported as critical modulators in many diseases including preeclampsia. Since the association between lncRNA BNIP3P1 and its cognate gene BNIP3 in preeclampsia has been revealed previously, this study aimed to further explore the function and mechanism of BNIP3P1 in preeclampsia. EdU and TUNEL assays revealed that BNIP3P1 or BNIP3 overexpression inhibited trophoblast cell proliferation and enhanced cell apoptosis in preeclampsia. As suggested by western blot analysis, the protein levels of apoptotic markers in the cells were affected by BNIP3P1 or BNIP3 overexpression. The binding between miR‐128‐3p and BNIP3P1 (or BNIP3) was explored by luciferase reporter assays. Mechanistically, BNIP3P1 bound to miR‐128‐3p to upregulate BNIP3 expression by acting as a competing endogenous RNA (ceRNA). Importantly, BNIP3P1 was found to inactivate the mTOR signaling pathway. In conclusion, BNIP3P1 inhibited trophoblast cell proliferation and enhanced cell apoptosis in preeclampsia by targeting the miR‐128‐3p/BNIP3/mTOR signaling pathway. [ABSTRACT FROM AUTHOR]

Preeclampsia (PE) is the leading cause of maternal and fetal mortality and morbidity. Furthermore, recent studies have reported that miR-145 within the preeclamptic trophoblast debris may cause the high blood pressure via interacting with the maternal endothelium. The aim of the present study was to investigate the functions of miR-145 in PE. Reverse transcription-quantitative polymerase chain reaction and western blotting were used to assess the expression of miR-145 and mucin (MUC1), respectively. TargetScan, miRBase and miRWalk were used to predict the targets of miR-145. Constructed miR-145 mimic plasmids were transfected into HTR-8/SVneo cells for further experiments, including an MTT assay for cell proliferation, Transwell assay for cell invasion and flow cytometry for cell apoptosis analysis. Additionally, the luciferase reporter gene system was employed for target verification. The results demonstrated that miR-145 is downregulated and MUC1 is upregulated in PE tissues and cells compared with normal placenta tissues and cells. The correlation analysis suggests that the expression of miR-145 is negatively correlated with MUC1. Meanwhile, increased proliferation, enhanced invasion and decreased apoptosis of HTR-8/SVneo cells was observed in miR-145 mimic groups compared with mimic control group. Also, the decreased luciferase activity in the miR-145 mimic group indicates that MUC1 may be a target of miR-145. In summary, the results of the present study suggest that miR-145 may serve key roles in the regulation of trophoblast cell proliferation and invasion by targeting MUC1. [ABSTRACT FROM AUTHOR]