Overview
- A genome-wide CRISPR screen of ErSO-treated cells identified FGD3 as the top genetic determinant of sensitivity.
- Raising or lowering FGD3 levels controlled ErSO killing in 2D cell lines, patient-derived organoids, and a mouse model.
- FGD3 reorganizes actin to weaken cell architecture so drug-swollen cancer cells rupture, releasing signals that recruit natural killer cells and macrophages.
- Retrospective patient datasets showed higher FGD3 correlated with better responses to multiple chemotherapies, including doxorubicin and epirubicin.
- The peer-reviewed study in the Journal of Experimental & Clinical Cancer Research presents FGD3 as a predictive biomarker, with ErSO still preclinical and prospective clinical validation and safety assessment needed given context-dependent effects.