• miR-194-3p is significantly upregulated during TGF-β-induced EMT in embryonic epicardial cells, and its overexpression promotes EMT while its inhibition attenuates the process.
• miR-194-3p directly targets p120-catenin, negatively regulating its expression, which in turn modulates β-catenin levels and the cell adhesion pathway.
• Silencing p120-catenin rescues the EMT suppression caused by miR-194-3p inhibition, confirming the mechanistic link.
• These findings highlight miR-194-3p as a potential therapeutic target for cardiac repair and regeneration, given its role in epicardial EMT.
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