GSE168497
LncRNA APTR promotes uterine leiomyoma cell proliferation by targeting ERa to activate the Wnt/ß-catenin pathway
The molecular mechanisms by which uterine leiomyoma (UL) cells proliferate are unclear. Long noncoding RNA (lncRNA) is reported to participate in the occurrence and development of gynecological cancers. We investigated the molecular mechanisms that lncRNA uses in UL. We found that lncRNA Alu-mediated p21 transcriptional regulator (APTR) showed higher expression in UL tumor tissues compared with that in normal uterine tissues. APTR induced cell proliferation and colony formation both in vitro and in vivo. The JASPAR database showed that APTR was likely interacted with ERa, and these molecules were identified via laser scanning confocal microscopy and RNA immunoprecipitation analysis. To verify the correlation between APTR and ERa, we overexpressed and underexpressed APTR and simultaneously expressed ERa. The results showed that APTR function was suppressed. APTR increased the expressions of the proteins in the Wnt pathway, and inhibiting ERa eliminated these responses. In conclusion, our data suggest that APTR promoted leiomyoma cell proliferation through the Wnt pathway by targeting ERa, suggesting a new role of APTR in the Wnt signaling pathway in UL. Overall design: Three patients were included in the study, and UL tumor tissue and adjacent normal uterine tissue specimens were acquired at the follicular phase. Inclusion criteria for this study were patients who (a) were nonmenopausal, (b) had undergone a hysterectomy because of UL between 12/2016 and 08/2017, (c) were without medical complications, and (d) had no history of hormone therapy.