Signal transducers and activators of transcription 5B potentiates v-Src-mediated transformation of NIH-3T3 cells

Previously, we reported that whereas both signal transducers and activators of transcription (STAT) 5A and STAT5B can be activated with respect to tyr osine phosphorylation and DNA binding potential by Src kinase, only STAT5B was translocated to the nucleus, where it presumably activates unique downs tream responses. To help elucidate the functional consequences of STAT5B ac tivation by v-src, the properties of stably transfected NIH-3T3 cells conta ining both an intact and a dominant negative, COOH-terminal-truncated isofo rm of STAT5B were investigated. STAT5B enhanced the transforming potential of v-Src as reflected by both an increase in focus formation and growth in soft agar, STAT5B also enhanced v-Src-induced cell cycle progression and ce ll motility in NIH-3T3 cells. Furthermore, the dominant negative, COOH-term inal-truncated isoform of STAT5B was able to partially suppress v-Src-media ted cell transformation. These results support the hypothesis that STAT5B m ay enhance Src/Abl-induced tumorigenesis. Accordingly, the equilibrium betw een STAT5B and STAT5A and their naturally occurring truncated forms may the refore play a key role in the etiology of certain cancers.