Prostate cancer (PCa) remains a significant health threat, with chemoresistance and recurrence posing major challenges despite advances in treatment. The epithelial to mesenchymal transition (EMT), a biochemical process where cells lose epithelial features and gain mesenchymal traits, is linked to chemoresistance and metastasis. Electrical impedance spectroscopy (EIS), a novel label-free electrokinetic technique, offers promise in detecting cell phenotype changes. In this study, we employed EIS to detect EMT in prostate cancer cells (PCCs). PC3, DU145, and LNCaP cells were treated with EMT induction media for five days. EIS characterization revealed unique impedance spectra correlating with metastatic potential, distinguishing DU145 EMT+ and EMT− cells, and LNCaP EMT+ and EMT− cells (in combination with dielectrophoresis), with comparisons made to epithelial and mesenchymal controls. These changes were supported by shifts in electrical signatures, morphologies, and protein expression, including the downregulation of E-cadherin and upregulation of vimentin. No phenotype change was observed in PC3 cells, which maintained a mesenchymal phenotype. EMT+ cells were also distinguishable from mixtures of EMT+ and EMT− cells. This study demonstrates key advancements: the application of EIS and dielectrophoresis for label-free EMT detection in PCCs, characterization of cell electrical signatures after EMT, and EIS sensitivity to EMT transitions. Detecting EMT in PCa is important to the development of more effective treatments and overcoming the challenges of chemoresistance.

Prostate cancer (PCa) remains a significant health threat, with chemoresistance and recurrence posing major challenges despite advances in treatment. The epithelial to mesenchymal transition (EMT), a biochemical process where cells lose epithelial features and gain mesenchymal traits, is linked to chemoresistance and metastasis. Electrical impedance spectroscopy (EIS), a novel label-free electrokinetic technique, offers promise in detecting cell phenotype changes. In this study, we employed EIS to detect EMT in prostate cancer cells (PCCs). PC3, DU145, and LNCaP cells were treated with an EMT induction media for five days. EIS characterization revealed unique impedance spectra correlating with metastatic potential, distinguishing DU145 EMT+ and EMT-cells, and LNCaP EMT+ and EMT-cells (in combination with dielectrophoresis), with comparisons made to epithelial and mesenchymal controls. These changes were supported by shifts in electrical signatures, morphological, and protein expression, including downregulation of E-cadherin and upregulation of vimentin. No phenotype change was observed in PC3 cells, which maintained a mesenchymal phenotype. EMT+ cells were also distinguishable from mixtures of EMT+ and EMT-cells. This study demonstrates key advancements: application of EIS and dielectrophoresis for label-free EMT detection in PCCs, characterization of cell electrical signature after EMT, and EIS sensitivity to EMT transitions. Detecting EMT in PCa is important to the development of more effective treatments and overcoming the challenges of chemoresistance.