Objective: Pre-eclampsia (PE) is a major complication of pregnancy, but its pathogenesis is unclear. This study explored the role of LINC01128 in the progression of PE, and its interaction with miR-16 on the behaviors of trophoblasts.Methods: The mRNA levels of LINC01128 and miR-16 in placental tissues and HTR-8/SVneo cells were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit (CCK)-8, wound healing assay and transwell assay were used to detect proliferation, migration and invasion. E-Cadherin, Vimentin, Matrix metalloproteinase 2 (MMP2) and MMP9 protein expressions were detected by Western blot. The correlation between LINC01128 and miR-16 was determined and verified by starBase and dual-luciferase assay.Results: The expression of LINC01128 was downregulated in PE. Overexpression of LINC01128 promoted LINC01128 expression, cell proliferation, migration, invasion and the expressions of Vimentin, MMP2 and MMP9, but inhibited the expression of E-Cadherin. SiLINC01128 showed opposite effects. MiR-16 interacted with LINC01128, and miR-16 was high-expressed in PE placentae. MiR-16 inhibitor promoted cell proliferation, migration, invasion and related protein expressions, but inhibited the expression of E-Cadherin. However, siLINC01128 inhibited the regulatory effect of miR-16 inhibitor on HTR-8/Svneo cells.Conclusion: LINC01128/miR-16 is involved in HTR-8/SVneo cells by regulating the migration and invasion of human chorionic trophoblast cells.
Keywords: Cell invasion; LINC01128; MicroRNA-16; cell migration; pre-eclampsia.