Synthesis of proto-oncogene proteins and cyclins depends on intact microfilaments

Focal adhesion signaling and actin stress fibers are dispensable for progression through the ongoing cell cycle

“…Our results show that these cells can progress through the ongoing cell cycle independent of stress fiber formation and the corresponding spread cell shape. This observation seems to be in contrast with a number of studies demonstrating G1 arrest Journal of Cell Science 120 (1) upon disruption of the actin cytoskeleton in a variety of cells (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;Reshetnikova et al, 2000;Bottazzi et al, 2001;Huang and Ingber, 2002;Lohez et al, 2003). The majority of these reports, however, focused on cells entering G1 phase from quiescence, demonstrating that cytoskeletal disorganization blocks events crucial to resume proliferation at the G0-G1 border such as downregulation of p27 KIP1 , activation of the p42/p44 MAPKs and the induction of cyclin D1 Huang et al, 1998;Bottazzi et al, 2001;Huang and Ingber, 2002).…”

“…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.…”

Graphene oxide and reduced graphene oxide induced neural pheochromocytoma-derived PC12 cell lines apoptosis and cell cycle alterations via the ERK signaling pathways

“…Matesanz et al 32 attributed the GO-induced cell cycle alterations to the location of GO on F-actin filaments because actin microfilaments must be intact for G1 progression, S phase entry, and mitotic division. 34 However, the detailed molecular mechanism remains unknown. Therefore, we explored changes in ERK signaling pathway molecules after exposure to 50 µg/mL GO and rGO.…”

Cytoskeletal Organization and Rb Tumor Suppressor Gene

“…However, the levels of p21 CIP1 and p27 KIP1 were not affected under the same treatment. Fasshauer et al suggested that disorganization of actin filaments using latrunculin A, latrunculin B, or cytochalasin D leads to reduction of c-jun and cyclin (D1, E, A) expression and inhibition of entry into S phase (131). Interestingly, Rb and p107 double-null mouse embryo fibroblasts (MEFs) are able to reach mid-G1 phase without serum stimulation, whereas they can not transit to the S phase without anchorage (121).…”