ArticleMolecular therapy. Oncology2026
The miR-16-1-3p suppresses proliferation and invasiveness via the MDM2-p53 axis in TGF-β1 signaling in osteosarcoma.
Article in Molecular therapy. Oncology, 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
The TGF-β signaling pathway has both tumor-suppressive and metastasis-promoting effects in cancer, yet the molecular determinants governing this switch remain unclear. Here, we investigated the miR-16-1-3p/MDM2/p53 axis as a potential regulator of TGF-β/Smad signaling output in osteosarcoma. miR-16-1-3p overexpression alone markedly reduced the proliferative and clonogenic potential of U2OS cells, while its combination with TGF-β treatment strongly enhanced G1-phase arrest and nearly abolished tumor growth capacity. miR-16-1-3p inhibited TGF-β-induced actin remodeling and epithelial-mesenchymal transition (EMT)-associated changes. While TGF-β promoted both 2D and 3D migration, miR-16-1-3p overexpression, alone or combined with TGF-β, counteracted its pro-migratory effects. Mechanistically, miR-16-1-3p reduced MDM2 expression and stabilized p53, which was associated with enhanced p21 induction and suppression of proliferative responses under TGF-β stimulation. Co-administration of TGF-β and miR-16-1-3p markedly increased cisplatin sensitivity in wild-type U2OS cells and reduced tumor nodule volume, Ki67 expression, and metastasis in the chicken chorioallantoic membrane model. Collectively, these findings suggest that miR-16-1-3p biases TGF-β signaling output toward anti-growth responses, while attenuating pro-migratory effects through MDM2 inhibition and p53 stabilization, providing a mechanistic rationale for improving therapeutic responses in osteosarcoma.
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