MiR-551b-5p deficiency associates with malignant phenotypes in gastric cancer: potential mediation by TRAF6.

The inflammatory tumor microenvironment (i-TME) significantly impacts the prognosis of gastric cancer (GC). Cytokines such as IL-6 may contribute to adverse phenotypes in GC; however, their regulatory mechanisms remain unclear. The role of miR-551b-5p in other cancers suggests it can target inflammation-related genes to regulate the i-TME and influence tumor prognosis. The present study aimed to investigate whether miR-551b-5p regulates the i-TME in GC and affects GC prognosis. Reverse transcription-quantitative PCR (RT-qPCR), western blotting, dual-luciferase reporter assays, cell scratch wound healing assays, Annexin V-FITC/PI double staining and in vitro angiogenesis assays were employed to investigate the differential expression of miR-551b-5p and TNF receptor-associated factor 6 (TRAF6) between GC tumors and normal tissues, and to explore the relationship between their expression levels and inflammatory cytokines. Prognostic analysis, immune infiltration assessment, oncogenic pathway analysis and single-cell Uniform Manifold Approximation and Projection analysis were used to validate the relationship between IL-6 and malignant phenotypes in GC. Experimental results demonstrated a significant deficiency of miR-551b-5p expression in GC. miR-551b-5p was found to target and inhibit TRAF6. Overexpression of TRAF6 was associated with increased IL-6 expression within the inflammatory microenvironment, and correlated with enhanced tumor cell proliferation, invasion, and poorer prognosis in gastric cancer. Deficiency of miR-551b-5p may lead to TRAF6 overactivation, which is associated with elevated IL-6 levels and malignant phenotypes in gastric cancer. miR-551b-5p and TRAF6 may serve as crucial molecular targets for GC therapy and prognostic prediction.