ETS1 SUPPRESSES TUMORIGENICITY OF HUMAN COLON-CANCER CELLS

We have ectopically expressed transcription factor ETS1 in two differe nt highly tumorigenic human colon cancer cell lines, DLD-1 and HCT116, that do not express endogenous ETS1 protein and have obtained several independent clones. The expression of wild-type ETS1 protein in these colon cancer cells reverses the transformed phenotype and tumorigenic ity in a dose-dependent manner. By contrast, expression in DLD-1 cells of a variant form of ETS1, lacking transcriptional activity, did not alter the tumorigenic properties of the cells, suggesting that the red uction in tumorigenicity in these clones was specific for the wild-typ e ETS1 gene products. Since these colon cancer cells have multiple gen etic alterations, the system described in this paper could be a good m odel to study-the Suppression of tumorigenicity at a transcriptional l evel, which could lead to the design and development of novel drugs fo r cancer treatment.