LncRNA VPS9D1-AS1 Sponging miR-520a-5p Contributes to the Development of Uterine Corpus Endometrial Carcinoma by Enhancing BIRC5 Expression.

Abstract

The pattern of VPS9D1-AS1 expression and its effects on uterine corpus endometrial carcinoma (UCEC) remained unclear. VPS9D1-AS1, miR-520a-5p, and BIRC5 mRNA levels were quantified by qRT-PCR. Bax, Bcl-2, N-cadherin, E-cadherin, and BIRC5 protein levels were analyzed through western blotting. Cell migration, invasion, proliferation, as well as apoptosis of cells were checked after performing assay for wound-healing, Transwell, cell-counting kit-8 (CCK-8) assay, and western blotting. VPS9D1-AS1 effects on UCEC were observed in nude mice. Through bioinformatics tools, we analyzed the association present among miR-520a-5p, BIRC5, and VPS9D1-AS1 along with RNA immunoprecipitation, and Dual-Luciferase verification reporter analysis. Our findings suggested VPS9D1-AS1 gene expression was up-regulated in both tissues as well as cells of UCEC. VPS9D1-AS1 knockdown suppressed migration, invasion, epithelial-mesenchymal transition (EMT) along with proliferation of UCEC cells, caused in vitro cell apoptosis initiation, and in vivo reduction of tumor growth. Mechanistically, it was verified that VPS9D1-AS1 targeted BIRC5 and caused miR-520a-5p sponging. Inhibitor of miR-520-5p markedly reversed the anti-tumor effects of VPS9D1-AS1 knockdown or BIRC5 knockdown on UCEC progression. Our studies revealed that VPS9D1-AS1 contributed to the UCEC development and progression by binding to miR-520a-5p competitively and inducing BIRC5 expression, indicating that VPS9D1-AS1 might act as a therapeutic target to develop new therapies for UCEC patients.