miR-3662 targets CAB39L to promote proliferation and invasion in gastric cancer.

Gastric cancer (GC) represents a highly aggressive malignancy within the gastrointestinal tract. The expression of miR-3662 exhibits specificity across different tumor types, but its precise biological role in GC pathogenesis remains poorly understood. Based on the results of bioinformatics analysis, we observed that miR-3662 was significantly overexpressed in GC. Subsequently, we investigated the biological role of miR-3662 in regulating the malignant phenotype of GC cells. Bioinformatics prediction combined with dual-luciferase assay confirmed that CAB39L is a direct target of miR-3662. Functional gain- and loss-of-function experiments were conducted to explore the impact of the miR-3662/CAB39L axis on the malignant characteristics of GC cells, as well as its influence on the activation of the AMPK signaling pathway and the expression of key glycolytic proteins. The results demonstrated that miR-3662 overexpression enhanced the proliferation, invasion, and migration of AGS cells, upregulated the expression of PFKP and LDHA, while suppressing apoptosis and reducing AMPK phosphorylation. Conversely, silencing miR-3662 exhibited opposing effects in HGC-27 cells. CAB39L expression was found to be downregulated in GC tissues. Upregulation of CAB39L inhibited GC cell proliferation, invasion, and migration, decreased the expression of PFKP and LDHA, and increased both apoptosis and AMPK activation. Furthermore, overexpression of CAB39L partially counteracted the promoting effects of high levels of miR-3662 on the malignant biological phenotype of GC cells. In conclusion, this study reveals that miR-3662 acts as a carcinogenic regulator in GC by targeting CAB39L, with the underlying mechanism potentially involving the modulation of AMPK activation to enhance cellular glycolysis.