ArticleFrontiers in genetics2026
The miR-16-1-3p passenger strand exhibits functional activity and suppresses malignant phenotypes in osteosarcoma.
Article in Frontiers in genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Chemotherapy resistance and disease progression remain major causes of mortality in osteosarcoma (OS). The miR-16 family is linked to tumors, but the specific function and treatment potential of the miR-16-1-3p passenger strand in OS remain unclear. Methods: RNA sequencing and clinical data from 82 OS patients in the TARGET-OS cohort were analyzed. Patients were stratified by progression status. Target genes of miR-16-1-3p were predicted using TargetScan and evaluated by gene set enrichment analysis (GSEA). Principal component analysis (PCA) and Kaplan-Meier survival analyses were performed based on cumulative Z-score-derived expression of the target gene set. Functional enrichment was assessed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. The impact of lentivirus-transduced miR-16-1-3p on U2OS cells was examined, focusing on proliferation, cell cycle, migration, colony formation, cisplatin sensitivity, and tumor growth in the CAM Results: GSEA demonstrated significant enrichment of predicted miR-16-1-3p target genes among genes upregulated in patients with progressive disease. Kaplan-Meier analysis showed that elevated cumulative expression of predicted miR-16-1-3p target genes was associated with poorer overall survival in osteosarcoma patients. GO and KEGG analyses revealed enrichment of pathways related to translational regulation, mitochondrial function, and chemotherapy-associated signaling. A fluorescent miR-16-1-3p sensor system demonstrated sequence-dependent suppression of reporter activity following miR-16-1-3p overexpression. In functional assays performed in both U2OS and HOS cells, miR-16-1-3p overexpression significantly suppressed proliferation and migration and increased cisplatin sensitivity compared with control (scrambled miRNA) virus-transduced cells. Quantitative PCR and luciferase reporter assays further supported the interaction of miR-16-1-3p with SLC38A1 and ABCA13, two candidate genes potentially associated with chemoresistance. Conclusion: The miR-16-1-3p passenger strand exhibited functional activity associated with tumor-suppressive phenotypes and increased cisplatin sensitivity in osteosarcoma cells. Using integrative bioinformatics, fluorescent sensor assays, and functional experiments in U2OS and HOS cells points to miR-16-1-3p possibly regulating cancer characteristics and how osteosarcoma reacts to chemotherapy.
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