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Updated: Dec 13, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
PTEN suppresses epithelial-mesenchymal transition and cancer stem cell activity by downregulating Abi1
Yanmei Qi1, Jie Liu1, Joshua Chao1
1Department of Surgery, Rutgers University Robert Wood Johnson Medical School, 125 Paterson Street, MEB-687, New Brunswick, NJ, 08093, USA.
Abstract:
The epithelial-mesenchymal transition (EMT) is an embryonic program frequently reactivated during cancer progression and is implicated in cancer invasion and metastasis. Cancer cells can also acquire stem cell properties to self-renew and give rise to new tumors through the EMT. Inactivation of the tumor suppressor PTEN has been shown to induce the EMT, but the underlying molecular mechanisms are less understood. In this study, we reconstituted PTEN-deficient breast cancer cells with wild-type and mutant PTEN, demonstrating that restoration of PTEN expression converted cancer cells with mesenchymal traits to an epithelial phenotype and inhibited cancer stem cell (CSC) activity. The protein rather than the lipid phosphatase activity of PTEN accounts for the reversal of the EMT. PTEN dephosphorylates and downregulates Abi1 in breast cancer cells. Gain- and loss-of-function analysis indicates that upregulation of Abi1 mediates PTEN loss-induced EMT and CSC activity. These results suggest that PTEN may suppress breast cancer invasion and metastasis via dephosphorylating and downregulating Abi1.
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