LncRNA OIP5-AS1 promotes immune evasion in abdominal aortic aneurysm cells by recruiting MDSCs and inhibiting CD8 + T cells through STK24 upregulation.

This study aims to investigate the expression and immune function of long non-coding RNA OIP5-AS1 (OIP5-AS1) and Serine/Threonine Kinase 24 (STK24) in abdominal aortic aneurysm (AAA). An animal model of AAA was established, along with cell models for overexpression and underexpression of OIP5-AS1 and STK24. Histological staining, qPCR, enzyme-linked immunosorbent assay (ELISA), Cell Counting Kit-8 assay, western blotting, RNA immunoprecipitation (RIP) analysis, and flow cytometry were employed to assess their effects on inflammation, cell proliferation, and apoptosis. In this study, Immunohistochemistry and qPCR analyses revealed significant upregulation of OIP5-AS1 and STK24 in both AAA tissue samples as well as cell models. ELISA demonstrated that elevated levels of OIP5-AS1 and STK24 significantly enhanced the secretion of inflammatory cytokines (IL-1β, IL-6, TNF-α, and IFN-γ), promoted cell proliferation while inhibiting apoptosis. RIP analysis combined with RNA pull-down assays indicated that OIP5-AS1 binds to the promoter region of STK24 by recruiting Zinc Finger Protein 93 (ZNF93) transcription factor leading to increased transcriptional expression of STK24. Furthermore, it was found that the functional role played by OIP5-AS1/STK24 axis operates through the AKT pathway. Increased expression levels of either OIP5-SAI or STK24 facilitated myeloid- derived suppressor cells (MDSCs) migration while suppressing CD8 + T-cell activity. The findings from this study highlight the critical involvement of the OIP5-SAI/STK24 axis in AAA progression by promoting MDSCs migration while inhibiting CD8 + T-cell activity. These insights provide novel perspectives into understanding the molecular pathology underlying AAA development while identifying potential therapeutic targets. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10616-025-00767-x.