title: Phase transitions in the growth of C3H 10T1/2 cells.
abstract: In systems used to express transformation using focus formation as the end point, nontransformed cells generally express a down-regulation of cell growth and division made evident by the formation of a monolayer of cells that completely covers the growth surface. In C3H 10T1/2 cells, down-regulation is thought to be progressively effected principally by cell-to-cell communication via gap junctions. Starting with a sparse population in asynchronous growth--e.g. containing cells in all phases of the growth cycle--as the area density increases, cells are progressively lost from the distribution in the order M phase, G2 phase, S phase and G1 phase, leading to the accumulation of viable cells out of cycle in so-called G0 phase. We have measured the progressive phase transitions as a function of inoculum size and time. The influence of a promoter and an antipromoter was also examined as well as the expression of the cyclin/cyclin-dependent kinase inhibitors p21Waf1/Cip1 and p27Kip1 as the cells grew into confluence. Using cells synchronized in mitosis, we found that with increasing cell density the expression of p27 increased and concomitantly p21 decreased.
authors.affiliation: Department of Radiological Health Sciences, Colorado State University, Fort Collins 80523, USA.
authors.forename: R L
authors.initials: RL
authors.lastname: Wells
authors.forename: Q
authors.initials: Q
authors.lastname: Hu
authors.forename: Y
authors.initials: Y
authors.lastname: Xing
authors.forename: W
authors.initials: W
authors.lastname: Buddenbaum
authors.forename: C K
authors.initials: CK
authors.lastname: Hill
authors.forename: M M
authors.initials: MM
authors.lastname: Elkind
mesh_terms: D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology; D002273:Carcinogens / Q000494:pharmacology; D018797:Cell Cycle Proteins; D002455:Cell Division / Q000528:radiation effects*; D002460:Cell Line; D002471:Cell Transformation, Neoplastic / Q000187:drug effects / Q000528:radiation effects; D050759:Cyclin-Dependent Kinase Inhibitor p21; D050760:Cyclin-Dependent Kinase Inhibitor p27; D016213:Cyclins / Q000235:genetics; D004307:Dose-Response Relationship, Radiation; D018499:Linear Energy Transfer; D051379:Mice; D008809:Mice, Inbred C3H; D008869:Microtubule-Associated Proteins / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D016196:S Phase / Q000528:radiation effects*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014212:Tretinoin / Q000494:pharmacology; D025521:Tumor Suppressor Proteins
chemical_list: D016588:Anticarcinogenic Agents; D002273:Carcinogens; C493957:Cdkn1a protein, mouse; C493961:Cdkn1b protein, mouse; D018797:Cell Cycle Proteins; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D008869:Microtubule-Associated Proteins; D012333:RNA, Messenger; D025521:Tumor Suppressor Proteins; D050760:Cyclin-Dependent Kinase Inhibitor p27; D014212:Tretinoin; D013755:Tetradecanoylphorbol Acetate