• HengXin Tang, Delong Zhu, Guozhi Zhang, Xiaoli Luo, and Wei Xie.
• Department of Neurosurgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China. Electronic address: thx201978@126.com.
• World Neurosurg. 2019 Oct 1; 130: e888-e898.

BackgroundWe 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.MethodsThe 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.ResultsAFAP1-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 the PI3K/AKT signaling pathway in rat pituitary adenoma cells.ConclusionWe found that AFAP1-AS1 and miR-103a-3p could be a potential therapeutic target for pituitary adenoma.Copyright © 2019 Elsevier Inc. All rights reserved.

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