EGFR/uPAR interaction as druggable target to overcome vemurafenib acquired resistance in melanoma cells.

ABSTRACT:

Background

BRAF inhibitor (BRAF-I) therapy for melanoma patients harboring the V600E mutation is initially highly effective, but almost all patients relapse within a few months. Understanding the molecular mechanisms behind BRAF-I responsiveness and acquired resistance is therefore an important issue. Here we assessed the role of urokinase type plasminogen activator receptor (uPAR) as a potentially valuable biomarker in the acquisition of BRAF-I resistance in V600E mutant melanoma cells.

Methods

We examined uPAR and EGFR levels by real time PCR and western blot analysis. uPAR loss of function was realized by knocking down uPAR by RNAi or using M25, a peptide that uncouples uPAR-integrin interaction. We investigated uPAR-β1integrin-EGFR association by co-immunoprecipitation a

SUBMITTER: Laurenzana A 

PROVIDER: S-EPMC6355443 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature