Disruption of P2Y2 Signaling Promotes Breast Tumor Cell Dissemination by Reducing ATP-Dependent Calcium Elevation and Actin Localization to Cell Junctions.

ABSTRACT: The tumor microenvironment and healing wounds both contain extremely high concentrations of adenosine triphosphate (ATP) compared to normal tissue. The P2Y2 receptor, an ATP-activated purinergic receptor, is typically associated with pulmonary, endothelial, and neurological cell signaling. Here, we examine ATP-dependent signaling in breast epithelial cells and how it is altered in metastatic breast cancer. Using rapid imaging techniques, we show how ATP-activated P2Y2 signaling causes an increase in intracellular Ca²⁺ in non-tumorigenic breast epithelial cells, approximately 3-fold higher than their tumorigenic and metastatic counterparts. The non-tumorigenic cells respond to increased Ca²⁺ with actin polymerization and localization to the cell edges after phalloidin

SUBMITTER: Mull ML 

PROVIDER: S-EPMC12071985 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature