AFAP1-AS1 Promotes Proliferation of Pituitary Adenoma Cells through miR-103a-3p to Activate PI3K/AKT Signaling Pathway

Abstract

We previously found that AFAP1-AS1 regulates the cell growth of pituitary tumor cells; however, the mechanism still remains unclear. Here, we investigated whether AFAP1-AS1 acts as a competing endogenous RNA of miR-103a-3p to regulate pituitary adenoma growth via the PI3K/AKT pathway. The bind between AFAP1-AS1 and rno-miR-103a-3p was measured by luciferase reporter assay, and rno-miR-103a-3p expression was measured by quantitative reverse transcription polymerase chain reaction. Proliferation, cell cycle, and apoptosis were measured by cell counting kit 8 and flow cytometry. Rat growth hormone (GH) and prolactin (PRL) levels in culture supernatant of GH3 and MMQ cells were measured by enzyme-linked immunosorbent assay. AFAP1-AS1 binds to rno-miR-103a-3p in rat pituitary adenoma cells. Additionally, rno-miR-103a-3p overexpression suppressed rat pituitary adenoma cell proliferation, induced cell apoptosis, arrested cell cycle in the G/S phase, reduced GH and PLR secretion, and inhibited the PI3K/AKT signaling pathway. Activated PI3K/AKT signaling pathway revised the effect of rno-miR-103a-3p overexpression on proliferation and GH and PLR secretion. Coexpression of both si-AFAP1-AS1 and rno-miR-103a-3p inhibitor promoted cell proliferation and cell cycle progression, reduced cell apoptosis, enhanced GH and PLR secretion, and activated thePI3K/AKT signaling pathway in rat pituitary adenoma cells. We found that AFAP1-AS1 and miR-103a-3p could be a potential therapeutic target for pituitary adenoma.