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Summary: Preeclampsia (PE) is a leading cause of maternal and perinatal death. Accumulated evidence suggests that many long non‐coding RNAs (lncRNAs) are abnormally expressed in placentas from PE patients, and they may play functional roles in the development of PE. The present study aimed to investigate the functional role TUG1 in PE and explore the potential molecular mechanisms. Clinically, the expression of TUG1 in placental tissues from PE and normal controls was determined. In vitro, human trophoblast HTR‐8/SVneo and JAR cells were employed for loss or gain‐of‐function assays. Our results demonstrate that TUG1 was downregulated in PE placental tissues compared with normal controls. Moreover, downregulation of TUG1 inhibited the migration and invasion of trophoblast‐like cells. Bioinformatics analysis and functional assays showed that TUG1 interacted with miR‐204‐5p and negatively regulated the expression and function of miR‐204‐5p in trophoblast cells. Furthermore, TUG1‐mediated migration and invasion of trophoblast cells was regulated by miR‐204‐5p. Together, our results suggested that TUG1 regulates trophoblast migration and invasion partly through sponging miR‐204‐5p, and the TUG1/miR‐204‐5p axis could be a potential therapeutic target for the treatment of PE. [ABSTRACT FROM AUTHOR]