miR-3913-3p promoted the progression of lung adenocarcinoma by regulating STX3 expression

Background The prognostic relevance and operational pathways of miR-3913-3p during disease advancement are not entirely clarified. This research intends to thoroughly assess the clinical importance and mechanistic contributions of miR-3913-3p within lung adenocarcinoma (LUAD) contexts. Methods Relationships linking miR-3913-3p abundance with five-year survival rates were examined through Kaplan-Meier methodology, while prognostic strength was determined by multivariate Cox regression modeling. Quantification of miR-3913-3p and STX3 in clinical specimens and cellular models was accomplished via RT-qPCR. Functional impacts on LUAD cells and regulatory interactions with target genes were validated through cell transfection, CCK-8 assays, Transwell migration/invasion assays, and dual-luciferase reporter assays. Results miR-3913-3p expression was significantly elevated in LUAD tissues compared to matched non-tumor tissues. High miR-3913-3p expression was significantly correlated with poor tumor differentiation, advanced TNM stage, and lymph node metastasis (p < 0.05). Multivariate Cox analysis identified high miR-3913-3p expression as a predictor of poor prognosis (HR = 2.450, 95% CI: 1.014–5.920, p = 0.046). Functionally, miR-3913-3p mimic enhanced the proliferative, migratory, and invasive capacities of LUAD cells, whereas miR-3913-3p inhibitor suppressed these malignant behaviors. Notably, co-transfection with si-STX3 rescued the inhibitory effects induced by the miR-3913-3p inhibitor. Mechanistically, dual-luciferase reporter assays confirmed that miR-3913-3p directly binds to the 3’untranslated region (3’UTR) of STX3, leading to its functional suppression. Conclusion This study demonstrates the existence of a regulatory miR-3913-3p/STX3 axis in LUAD. miR-3913-3p likely promotes the proliferation, migration, and invasion of LUAD cells by targeting STX3, implicating this axis in LUAD pathogenesis. Supplementary Information The online version contains supplementary material available at 10.1186/s41065-026-00654-1.