“…In addition to growth factors and adhesion, organization of the actin cytoskeleton is implicated in G1 phase progression since disruption of actin architecture with pharmacological agents leads to G1 arrest in a variety of cell types (Maness and Walsh, 1982;Ohta et al, 1985;Takasuka et al, 1987;Iwig et al, 1995;Bohmer et al, 1996;Fasshauer et al, 1998;Huang et al, 1998;Tsakiridis et al, 1998;Reshetnikova et al, 2000;Bottazzi et al, 2001;Huang and Ingber, 2002;Lohez et al, 2003). Cytoskeleton-dependent G1 arrest is mainly caused by a failure to induce sustained activity of the p42/p44 MAPKs, expression of cyclin D1 and downregulation of the cyclin-dependent kinase inhibitor p27 KIP1 Fasshauer et al, 1998;Huang et al, 1998;Bottazzi et al, 2001;Huang and Ingber, 2002), events that are required for quiescent cells to resume G1 phase progression upon growth factor stimulation (Baldin et al, 1993;Pages et al, 1993;Brondello et al, 1995;Sherr and Roberts, 1999). These studies have given rise to the concept that growth control in normal mammalian cells is dependent on cell spreading mediated by actin stress fibers.…”