Delay in serum stimulation of Erk activity caused by oncogenic transformation.

Mitogenic growth factor stimulation activates several signal transduction pathways, including the well-characterized Ras-Erk pathway, resulting in transient activation of Erk1 and Erk2. Oncogenic transformation, however, causes constitutive activation of growth signalling pathways, resulting in an accelerated rate of cell division. We investigated the effects of transformation on serum and growth factor stimulation of Erk1 and Erk2, and show that stimulation of these MAP kinases, as well as the Erk activator Mek, is delayed in oncogene transformed cells. Possible mechanisms of this delay are explored. In addition, our data indicate that prolonged mitogenic stimulation does not necessarily result in constitutive activation of Erk1 and Erk2.