Dysregulated pseudogene BNIP3P1 inhibited cell proliferation and promoted cell apoptosis in preeclampsia by acting as a competing endogenous RNA for BNIP3.

Abstract

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.