BVES-AS1 inhibits the malignant behaviors of colon adenocarcinoma cells via regulating BVES.

The underexpression of the long noncoding RNA (lncRNA) blood vessel epicardial substance antisense RNA 1 (BVES-AS1) has been shown in colon adenocarcinoma (COAD) patients. However, its role in COAD remains to be explored. This study aimed to investigate the function and potential mechanism of BVES-AS1 in COAD. Colony formation, Cell Counting Kit-8 (CCK-8), JC-1 mitochondrial membrane potential assay, wound healing, transwell, and western blot analyses were used to measure cell proliferation, apoptosis, migration, invasion and epithelial mesenchymal transition (EMT) in COAD cells. RNA pull-down, luciferase reporter and RNA binding protein immunoprecipitation (RIP) assays were used to detect the interaction of BVES-AS1 and downstream genes. BVES-AS1 was expressed at low levels in COAD cells. Overexpressed BVES-AS1 inhibited COAD cell proliferation, migration, invasion and EMT while elevating cell apoptosis. Mechanistically, BVES-AS1 functioned as a competing endogenous RNA (ceRNA) sponging miR-522-3p to regulate the expression of nearby gene blood vessel epicardial substance (BVES). Besides, BVES-AS1 recruited TATA-box binding protein associated factor 15 (TAF15) to promote BVES mRNA stability. Taken together, our study confirmed that BVES-AS1 inhibited COAD progression via interacting with miR-522-3p and TAF15 to regulate BVES expression, which might offer perspective for COAD treatment. This article is protected by copyright. All rights reserved.