circSLC39A8 by sponging hsa-miR-11181-5p and direct binding to PIK3CA mRNA promotes retinoblastoma proliferation

<b>Background:</b> Retinoblastoma (RB) is a prevalent intraocular malignant tumor, posing a significant threat to human life and health. Although the involvement of circRNAs in various malignancies has been reported, their precise role in RB remains incompletely understood. <b>Methods:</b> High-throughput sequencing was utilized to construct differential expression profiles of circRNAs, followed by candidate gene screening using RT-qPCR. The circular structure of circSLC39A8 was confirmed through stability assays with RNase R and Act D. A research system for transiently silencing and overexpressing circSLC39A8 was established, with flow cytometry employed to assess cell cycle and apoptosis levels. Bioinformatics analyses, RT-qPCR, and western blot experiments were conducted to evaluate the expression of circSLC39A8, hsa-miR-11181-5p, and PIK3CA. RNA antisense purification experiments were performed to elucidate interactions among circSLC39A8, hsa-miR-11181-5p, and PIK3CA. <b>Results:</b> Our findings revealed a significant upregulation of circSLC39A8 in RB. Functionally, circSLC39A8 was identified as promoting cellular proliferation and suppressing apoptosis <i>in vitro</i>, thereby facilitating RB progression. Mechanistically, circSLC39A8 indirectly augmented the expression levels of PIK3CA mRNA by acting as a competitive endogenous RNA for hsa-miR-11181-5p, consequently enhancing the stability of PIK3CA mRNA and ultimately fostering RB cell proliferation while inhibiting apoptosis.