MIR193BHG inhibits the proliferation, migration and invasion of trophoblasts by upregulating p53
Aberrantexpression of long non-coding RNAs (lncRNAs) has been reported to play a crucial role in the biological function of trophoblasts and contribute to preeclampsia (PE). Our previous study demonstrated that MIR193BHG is increased in preeclamptic placental tissues. In this study, we further explored the effects of  MIR193BHG on the function of trophoblast cells and attempted to elucidate its underlying molecular mechanisms. Results showed that MIR193BHG was predominantly localized in the nucleus of HTR-8/SVneo cells. Overexpression of MIR193BHG significantly inhibited proliferation, migration and invasion of HTR-8/SVneo cells, while increasing apoptosis. Knockdown of MIR193BHG produced opposite effects.Furthermore, overexpression of MIR193BHG led to significant increases in both mRNA and protein levels of p53 compared with the control group. More importantly, knockdown of p53 rescued the negative effects induced by overexpressed MIR193BHG on cell proliferation, migration, and invasion while partially counteracting its apoptotic effects on HTR-8/SVneo cells. In conclusion, our findings suggest that MIR193BHG played a critical role in the progression of PE by regulating the expression of p53 and  may serve as a novel therapeutic target for PE. Overall design: HTR-8/SVneo cells transfected with MIR193BHG overexpression plasmids and mock plasmids were collected and lysed with Trizol reagent. Next, 1µg RNA was used for library preparation with TruSeq Stranded Total RNA with Ribo-Zero Gold kit (Illumina). The sequenced reads were then aligned to the human reference genome (GRCh38.91) using Hisat2. Differential gene expression was performed using EdgeR. The threshold used in this study to screen up- or downregulated mRNAs was logFC > 0.5 and P < 0.05.