LncRNA uc003fir promotes CCL5 expression and negatively affects proliferation and migration of trophoblast cells in preeclampsia

•LncRNA uc003fir promotes CCL5 secretion.•Hypoxia increases the expression of lncRNA uc003fir.•lncRNA uc003fir promotes proliferation and migration of HTR-8/SVneo cells. To evaluate the role of lncRNA uc003fir in the progression and development of preeclampsia (PE). Paired test using placental tissue collected from PE women and normally pregnant women. First Hospital of Soochow University, Suzhou, China. 38 women with PE versus 42 normally pregnant women matched maternal and gestational age with the same-size ratio. Placental samples were analyzed using a human lncRNA microarray, and then the lncRNA uc003fir was validated by q-PCR. MTT, cell scratch, and transwell invasion assays were performed regarding biological functions. LncRNA uc003fir promoted CCL5 expression and negatively affected the proliferation and migration of HTR-8/SVneo cells. LncRNA uc003fir was significantly over-expressed in PE compared to the control. The chemokine CCL5 was directly regulated by lncRNA uc003fir through transfection of over-expression plasmid of lncRNA uc003fir in HTR-8/SVneo cells, accompanied by up-regulation of lncRNA uc003fir in preeclamptic placental vessels and vessel-free tissue. In detecting the biological function of lncRNA uc003fir on trophoblast cells, over-expression of lncRNA uc003fir increased proliferation, migration, and invasion of HTR-8/SVneo cells, whereas the knockdown inhibited. LncRNA uc003fir was dysregulated in placental tissue in PE. LncRNA uc003fir regulated CCL5 directly, which may mediate the recruitment of pro-inflammatory cytokines released from monocytes and other leukocytes. Additionally, lncRNA uc003fir may interact with microRNAs to affect the invasion of trophoblast cells into myometrium, indicating that lncRNA uc003fir could be considered as a target in PE.