The Bacterial Protein Azurin Impairs Invasion and FAK/Src Signaling in P-Cadherin-Overexpressing Breast Cancer Cell Models

摘要: P-cadherin overexpression occurs in about 30% of all breast carcinomas, being a poor prognostic factor for cancer patients. In cellular background wild-type E-cadherin, we have previously shown that its expression promotes invasion, motility and migration cells due to the induced secretion metalloproteases (MMPs) extracellular medium concomitant shedding pro-invasive soluble form this protein (sP-cad). Azurin is secreted by Pseudomonas aeruginosa induces vitro vivo cytotoxicity after preferential penetration human relative normal cells. Three different cell lines, MCF-7/AZ.Mock, MCF-7/AZ.Pcad SUM149 were treated with sub-killing doses azurin. Invasion these was measured using Matrigel Assays MTT assays performed determine viability upon treatment effects on cadherins determined Western blot Immunofluorescence. Gelatin Zymography used activity MMP2 conditioned media azurin untreated phosphorylation levels intracellular signaling proteins blot. The invasive phenotype significantly reduced (50–100 µM) also caused specific decrease from 30–50% but E-cadherin remain unaltered. More, sP-cad observed both FAK Src proteins. Our data show specifically targets P-cadherin, not abrogating P-cadherin-mediated signaling. Therefore, could possibly be considered therapeutic tool treat poor-prognosis carcinomas overexpressing wild type context.