Thus, a talin R8 K1530E/K1544E double mutant markedly reduced binding to DLC1 peptides in vitro, and to full-length DLC1 in cells, compromising the ability of GST-talin R8 constructs to displace DLC1 from endogenous talin and thereby to attenuate the tumor-suppressor activity of DLC1. Here, DLC1 is linked to neoplasm.