Expression of the human cDNA encoding the intermediate filament protein vimentin induces reversion of nitrosylmethylurea (NMU) transformed Syrian hamster kidney fibroblasts (NMU 34m cells) to a normal phenotype as assessed by morphology, anchorage independent growth parameters, and suppression of the tumorigenic phenotype and is apparently required for maintenance of the normal phenotype in BHK SN-10 cells. NMU 34m cells are transformed by inactivation of a tumor suppressor gene. BHK cells that are transformed as a result of infection by a tumor virus or by the introduction of an activated human oncogene also exhibit tumorigenic properties similar to NMU 34m cells. Expression of the human vimentin cDNA is not sufficient to revert virally or oncogene transformed BHK cells. Therefore vimentin functions in a manner analogous to a tumor suppressor gene in that its suppressive effects are restricted to cells transformed by recessive mechanisms.
