LncRNA SNHG16 regulates trophoblast functions by the miR-218-5p/LASP1 axis

Altered placental development and function lead to placental diseases such as preeclampsia (PE) which is mainly characterized by insufficient trophoblast invasion and abnormally invasive placenta disorders. Long noncoding RNAs (lncRNAs) are widely reported to function as crucial players in the pathogenesis of PE. The present investigation clarified the role of lncRNA small nucleolar RNA host gene 16 (SNHG16) in PE. RT-qPCR was used to measure gene expression. The proliferation of trophoblast cells was examined using CCK-8 and EdU assays. Trophoblast migration and invasion were assessed using wound healing and transwell assays. The apoptosis was estimated by flow cytometry. Luciferase reporter and RNA pull-down assays were performed to explore the molecular mechanisms in trophoblast cells. We found that SNHG16 was downregulated in placenta from patients with PE. Moreover, SNHG16 depletion significantly inhibited trophoblast cell proliferation, migration, and invasion and stimulated apoptosis, while SNHG16 overexpression exerted an opposite effect. Subsequently, we confirmed that SNHG16 acted as a competing RNA (ceRNA) of miR-218-5p that was verified to directly target LASP1. Both miR-218-5p depletion and LASP1 upregulation antagonized the effect of SNHG16 knockdown on HTR-8/SVneo cell functions. In conclusion, SNHG16 facilitates trophoblast cell migration and invasion by the miR-218-5p/LASP1 axis.