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Background: Mechanically gated PIEZO channels lead to an influx of cations, activation of additional Ca²⁺ channels, and cell depolarization. This study aimed to investigate PIEZO2’s role in breast cancer. Methods: The clinical relevance of <i>PIEZO2</i> expression in breast cancer patient was analyzed in a publicly available dataset. Utilizing <i>PIEZO2</i> overexpressed breast cancer cells, and <i>in vitro</i> and <i>in vivo</i> experiments were conducted. Results: High expression of <i>PIEZO2</i> was correlated with a worse survival in triple-negative breast cancer (TNBC) but not in other subtypes. Increased PEIZO2 channel function was confirmed in <i>PIEZO2</i> overexpressed cells after mechanical stimulation. <i>PIEZO2</i> overexpressed cells showed increased motility and invasive phenotypes as well as higher expression of SNAIL and Vimentin and lower expression of E-cadherin in TNBC cells. Correspondingly, high expression of <i>PIEZO2</i> was correlated with the increased expression of epithelial–mesenchymal transition (EMT)-related genes in a TNBC patient. Activated Akt signaling was observed in <i>PIEZO2</i> overexpressed TNBC cells. <i>PIEZO2</i> overexpressed MDA-MB-231 cells formed a significantly higher number of lung metastases after orthotopic implantation. Conclusion: PIEZO2 activation led to enhanced SNAIL stabilization through Akt activation. It enhanced Vimentin and repressed E-cadherin transcription, resulting in increased metastatic potential and poor clinical outcomes in TNBC patients.