Improving Ovarian Cancer Immunotherapy through Discoidin Domain Receptor 2 Blockade

Disease progression is supported by a tumour microenvironment (TME) enriched in dense collagen type I (Col1) fibres, promoting tumour growth and invasion while restricting T-cell infiltration. Discoidin domain receptor 2 (DDR2), a collagen-binding receptor tyrosine kinase, has emerged as a driver of tumour progression and immune exclusion, although its role in SOC immunotherapy resistance remains unclear.

Here we show that the inhibition of DDR2/Col1 interaction with WRG-28 in OVCA433 and OVCAR3 cells remodels the collagen matrix, favouring the recruitment, activation and cytotoxic activity of tumour-specific T cells.