miR-137 regulates autophagy and apoptosis in duodenal ulcer by targeting BNIP3L

Duodenal ulcer (DU) represents a clinical manifestation and disease state that occurs when the mucosal surface of the duodenum is damaged. The processes of autophagy and apoptosis have been linked to the development of DU, yet the precise roles they play remain unclear. This study aimed to investigate the expression and mechanism of action of microRNAs (miRNA)-137 (miR-137) in DU.

miR-137 is upregulated in DU patients and contributes to ulcer progression by inhibiting BNIP3L, reducing autophagy, and promoting apoptosis. Targeting miR-137 could provide a novel therapeutic strategy for DU management.

Dysregulated miRNAs and targeted genes were identified from the Gene Expression Omnibus database, and the immune cell infiltration levels were analyzed using CIBERSORT. To confirm the targeting of the miRNAs, we conducted dual luciferase reporter assays in vitro. The detection of cell apoptosis was conducted using flow cytometry. Moreover, quantitative reverse transcription polymerase chain reaction, cell counting kit-8, and Western blot were employed to ascertain the levels of autophagy- and apoptosis-related proteins.

Bioinformatics analysis identified 5 miRNAs, with miR-137 showing the most pronounced dysregulation. Its target gene, BNIP3L, was subsequently identified. In vitro experiments confirmed that miR-137 targeted BNIP3L. The upregulation of miR-137 expression in HIEC-6 cells resulted in the inhibition of BNIP3L expression, a reduction in autophagy, and an increase in apoptosis. A reduction in the expression of miR-137 would have the opposite effect. Conclusions: miR-137 is upregulated in DU patients and contributes to ulcer progression by inhibiting BNIP3L, reducing autophagy, and promoting apoptosis. Targeting miR-137 could provide a novel therapeutic strategy for DU management.