Urothelial cancer associated 1 (UCA1) regulates trophoblast viability, proliferation, and migration via modulating the UCA1/miR-455/RUNX2 signaling pathway.

Abstract

Spontaneous abortion (SA) is the spontaneous loss of a pregnancy before 20 gestational weeks. The causes of SA are still largely unknown. Long noncoding RNA (lncRNA) urothelial cancer associated 1 (UCA1) plays an important role in cellular progress. However, there is no report focusing on the role of UCA1 in SA. Here, we revealed that, compared with that in clinical samples from elective induced abortion, UCA1 expression was decreased in samples from SA patients as shown by qPCR method. The results demonstrated that UCA1 might be involved in the progress of SA. Then, we found that knockdown of UCA1 reduced cell viability and inhibited cell proliferation and migration of HTR-8/SVneo trophoblast cells as shown by CCK8, EdU, and Transwell methods. Furthermore, we demonstrated that UCA1 could act as a molecular sponge for miR-455 in HTR-8/SVneo cells as shown by luciferase reporter system method. In addition, miR-455 inhibited cell viability, cell proliferation and migration via regulating RUNX2 in HTR-8/SVneo cells. Ultimately, we illustrated that UCA1 plays its role via absorbing miR-455, thus promoting RUNX2 expression in HTR-8/SVneo cells. Collectively, this study first revealed the role and mechanism of UCA1 in the growth and migration of HTR-8/SVneo cells, indicating its potential as a diagnostic biomarker and therapeutic target for SA.