Abstract
Despite the enormous development of medical technologies in recent decades, pituitary adenoma (PA) remains among the most refractory cancers in the world. Elucidating the molecular mechanisms underlying the pathology of PA is essential to identify new treatments for PA. In the present study, we found that IFNG-AS1 expression was significantly higher in PA tissues than in nontumor tissues via qRT-PCR and RNA fluorescence in situ hybridization (FISH). shRNA-mediated IFNG-AS1 knockdown in HP75 cells significantly inhibited tumor progression, and IFNG-AS1 overexpression remarkably promoted tumor progression. Epithelial splicing regulatory protein 2 (ESRP2) was demonstrated to be a target protein of IFNG-AS1 in PA; knocking down ESRP2 reversed the tumor-inhibitory effects of IFNG-AS1 knockdown, and overexpressing ESRP2 abolished the tumor-promoting effects of IFNG-AS1 overexpression in HP75 cells. In conclusion, our findings suggested that IFNG-AS1 may function as an oncogene in PA by interacting with ESRP2.
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