In the present study, the modulation of Amot-p130 expression revealed that Amot-p130 inhibited the cancer stem cell (CSC) potential of BCa, disrupting β-catenin stability by competing with Axin for binding to tankyrase (TNKS), leading to a further inhibition of cell proliferation and epithelial–mesenchymal transition (EMT) in BCa. The gene discussed is AMOT; the disease is cancer.