The role of the SIRPG-AS1/miR-3692-5p/STAT1 axis in recurrent pediatric anal fistula.

BACKGROUND

Pediatric anal fistula is a clinically distinct condition. Postoperative recurrence remains a major therapeutic challenge, as the underlying molecular mechanisms are poorly understood.

AIM: To investigate the potential role of the SIRPG-AS1/miR-3692-5p/STAT1 axis in pediatric anal fistula progression and recurrence through bioinformatics analysis and experimental validation.

METHODS

Bioinformatics analysis of the GSE157020 dataset identified differentially expressed long non-coding RNAs (lncRNAs). The downstream miRNAs and target genes were predicted using multiple databases. The regulatory axis was validated using RIP, RNA pull-down, and dual-luciferase reporter assays. Clinical relevance was assessed in serum from 80 primary and 25 recurrent pediatric idiopathic anal fistula cases, compared with 80 healthy controls. Functional studies were performed in TGF-β-treated CCD-18Co cells with genetic manipulations.

RESULTS

Analysis of database GSE157020, SIRPG-AS1 was found to be significantly upregulated in anal fistula tissues. The SIRPG-AS1/miR-3692-5p/STAT1 axis was identified, with SIRPG-AS1 regulating STAT1 expression by competitively binding to miR-3692-5p. Clinical sample analysis revealed significant changes in the expression levels of SIRPG-AS1, miR-3692-5p, and STAT1 (as assessed in serum) in pediatric patients with anal fistula, correlating with disease severity and recurrence. In vitro experiments showed that the SIRPG-AS1/miR-3692-5p/STAT1 axis was involved in TGF-β-induced fibrosis in CCD-18Co cells.

CONCLUSIONS

Our study suggests that the SIRPG-AS1/miR-3692-5p/STAT1 axis may play a role in pediatric anal fistula progression and recurrence. Further investigation into this axis could provide additional insights into the mechanisms underlying pediatric anal fistula.