Similarly, we found that the CXCR1/2 antagonist decreased CXCL8-induced HT-29 cell adhesion to fibronectin and laminin I. Adhesive interactions between αV integrin subunit on one hand and several proteins in the extracellular matrix on the other hand could form a molecular basis for tumor cell adhesion to wound surfaces. This evidence concerns the gene FN1 and neoplasm.