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Macrosomia is a common perinatal complication, with a series of adverse effects on newborns and pregnant women. However, the effects of long non‑coding RNAs (lncRNAs) on non‑diabetic fetal macrosomia (NDFMS) remain unclear. The aim of the present study was to investigate whether aberrant lncRNA expression in the placenta is involved in the pathogenesis of NDFMS and to elucidate its biological mechanisms. The expression profile of lncRNAs in the placentas of pregnant women with NDFMS was investigated using an Agilent Human LncRNA Microarray. Differentially expressed lncRNAs were selected for validation using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). Additionally, the function of lncRNA ubiquitin‑specific peptidase 2 antisense RNA 1 ( USP2‑AS1 ) was investigated using a trophoblast cell line. The results revealed that 763 lncRNAs were upregulated and 129 lncRNAs were downregulated in the placentas of women in the NDFMS group (|FC| ≥2.0). A total of 10 lncRNAs (|FC| ≥4.0, signal value ≥50) were selected for validation using two‑stage RT‑qPCR, indicating that the expression trends of the 10 differentially expressed lncRNAs in the NDFMS group (n=8 vs. 8 and 48 vs. 48) were consistent with the microarray data. In addition, a significant downregulation in the levels of lncRNA USP2‑AS1 was observed in both the microarray data and second‑stage verification. The overexpression of lncRNA USP2‑AS1 induced G1 phase cell cycle arrest and the number of cells entering S phase was reduced. In addition, the viability of HTR‑8/SVneo cells was significantly inhibited when lncRNA USP2‑AS1 was overexpressed. Therefore, these findings demonstrated that lncRNAs were significantly differentially expressed in the placentas of pregnant women with NDFMS and that the downregulation of lncRNA USP2‑AS1 may be involved in the pathogenesis of NDFMS, by promoting trophoblast cell viability.

Downregulation of lncRNA USP2‑AS1 in the placentas of pregnant women with non‑diabetic fetal macrosomia promotes trophoblast cell proliferation