Objective: The aim of this study was to explore the role of long non-coding RNA (lncRNA) TCL6 in preeclampsia (PE) development and to investigate its underlying mechanism.
Patients and methods: The expression of TCL6 in 42 placental tissues of PE pregnancies and normal pregnancies was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Receiver Operating Characteristic (ROC) curve was applied to explore the relationship between TCL6 expression, urine protein level, blood pressure and neonatal weight of PE pregnancies. The proliferation and cell cycle of trophoblast cells after TCL6 knockdown were detected by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. Moreover, the specific role of TCL6 in cell cycle was detected by Western blot.
Results: TCL6 was highly expressed in 42 placental tissues of PE pregnancies when compared with that of normal pregnancies. PE pregnancies with lower expression level of TCL6 exhibited significantly lower urinary protein level, as well as systolic and diastolic blood pressure than those with higher level. Besides, neonatal weight was significantly higher in PE pregnancies with lower expression level of TCL6. Meanwhile, downregulation of TCL6 resulted in remarkably increased proliferation and cell cycle of trophoblast cells. In addition, Western blot results indicated that TCL6 knockdown significantly upregulated CDK2 and downregulated PTEN in trophoblast cells.
Conclusions: TCL6 was highly expressed in placental tissues of PE patients. Overexpression of lncRNA TCL6 inhibited the proliferation of trophoblast cells and promoted PE development via targeting PTEN.