E2F1-induced PROX1-AS1 contributes to cell growth by regulating miR-424-5p/CPEB2 pathway in endometrial carcinoma

Background LncRNA PROX1 antisense RNA 1 (PROX1-AS1) has been demonstrated to be upregulated in several kinds of cancers and serves as an oncogene. However, its role in the development of endometrial cancer (EC) remains unknown. The objective of this paper was to study the expression pattern of PROX1-AS1 in EC, and to reveal PROX1-AS1 role in EC progression, as well as the underlying mechanism. Objective Bioinformatics method was applied to predict the binding sites between the transcription factor E2F1 and PROX1-AS1 promoter, and miR-424-5p and PROX1-AS1/CPEB2, and the targeting relationships were further verified by luciferase gene reporter assay, chromatin immunoprecipitation (ChIP) and RNA immunoprecipitation (RIP). The expression levels of E2F1 and PROX1-AS1 in cells were detected using qPCR and/or western blotting. The CCK-8 and colony formation assays were applied to determine cell growth and colony formation abilities. Results The results showed that PROX1-AS1 and E2F1 were highly expressed in EC cells. E2F1 promoted PROX1-AS1 expression via binding to the E1 part of PROX1-AS1 promoter, resulting in enhancements in cell growth and colony formation abilities. In addition, PROX1-AS1 targeted miR-424-5p and decreased miR-424-5p expression, which then induced a significant increase in CPEB2 expression. Conclusion In conclusion, this study uncovered that PROX1-AS1 induced by E2F1 promoted the cell viability in EC through increasing CPEB2 expression via targeting miR-424-5p.