FN1 and colorectal carcinoma: Similarly, disruption of the dysadherin-fibronectin interaction by deletion of the extracellular domain of dysadherin (ΔN-mutant) abrogated the dysadherin-induced increases in CRC survival, migration, and invasion (Figure 5G,H and Figure S10D); this dysadherin-induced aggressive phenotype was attenuated by fibronectin knockdown or FAK inhibition (Figure S10D-F).