Long noncoding RNA GAS6-AS2 sponges microRNA-493, thereby enhancing the malignant characteristics of breast cancer cells via upregulation of FUT4.

Long noncoding RNA (lncRNA) GAS6-AS2 serves as an oncogenic lncRNA in various types of human cancer. In this study, we attempted to examine the functions of GAS6-AS2 in breast cancer (BC) and explore the potential mechanisms involved. Reverse-transcription quantitative PCR was carried out to determine GAS6-AS2 expression in BC tissues and cell lines. Multiple functional experiments, including a Cell Counting Kit-8 assay, Transwell migration and invasion assays, and an in vivo nude-mouse xenograft experiment, were conducted to evaluate the effects of GAS6-AS2 in BC cells. GAS6-AS2 expression was high in BC tumors, manifesting a strong correlation with tumor size, lymph node metastasis, TNM stage, and shorter overall survival in patients with BC. A knockdown of GAS6-AS2 restricted BC cell proliferation, migration, and invasion in vitro and retarded tumor growth in vivo. With regard to its mechanism, GAS6-AS2 acted as a competing endogenous RNA that sponged microRNA-493 (miR-493), thereby increasing the expression of fucosyltransferase IV (FUT4). Either miR-493 inhibition or FUT4 upregulation abrogated the consequences of GAS6-AS2 knockdown in BC cells. These results revealed that GAS6-AS2 sponges miR-493 to enhance the malignant characteristics of BC in vitro and in vivo by increasing FUT4 expression. Thus, this lncRNA is an effective therapeutic target in BC and a promising diagnostic biomarker of this cancer.