title: Dimethyl sulfoxide restores contact inhibition-induced growth arrest and inhibits cell density-dependent apoptosis in hamster cells.
abstract: Most nontransformed cell lines respond to confluence by arresting the cell cycle in a viable G(1) phase, whereas immortalized cell lines growing in monolayer do not stop cell cycle progression in response to high cell density and are subjected to density-dependent apoptosis. We have examined the effects, in terms of cell growth, apoptosis, and expression of adhesion molecules of culturing contact inhibition-deficient hamster cells in the presence of dimethyl sulfoxide (DMSO). Addition of 1.5% DMSO to the growth medium for 96 h arrested Chinese hamster ovary (CHO) cells in the G(1) phase as a confluent monolayer, associated with a remarkable increase in the expression of the cyclin-dependent kinase inhibitor p27. Cells cultured in DMSO-containing medium showed increased levels of cadherins and alpha5beta1 and beta1 integrin complexes. Cell exposure to DMSO also reduced both cell density-dependent apoptosis and necrosis and resulted in increased Bcl-2 expression. These results converge to indicate that DMSO restores contact inhibition-induced growth arrest and prevents high-density-dependent apoptosis and suggest that the effect of DMSO may be mediated by intracellular signaling triggered by cell-extracellular matrix and cell-cell interactions. Both p27 and bcl-2 appear to be involved in the resumption of growth control accompanying cell adhesion in DMSO-exposed CHO cells.
authors.affiliation: Centre for Evolutionary Genetics, C.N.R., c/o Department of Genetics and Molecular Biology, University "La Sapienza,", Rome, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Fiore
authors.forename: F
authors.initials: F
authors.lastname: Degrassi
mesh_terms: D016475:3T3 Cells; D000818:Animals; D017304:Annexin A5 / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects*; D016466:CHO Cells; D015820:Cadherins / Q000378:metabolism; D002448:Cell Adhesion / Q000187:drug effects; D002450:Cell Communication / Q000187:drug effects; D002452:Cell Count; D018797:Cell Cycle Proteins; D002455:Cell Division / Q000187:drug effects; D003260:Contact Inhibition / Q000187:drug effects* / Q000502:physiology; D006224:Cricetinae; D050760:Cyclin-Dependent Kinase Inhibitor p27; D053938:DNA Fragmentation / Q000187:drug effects; D004121:Dimethyl Sulfoxide / Q000494:pharmacology*; D004847:Epithelial Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D005109:Extracellular Matrix / Q000187:drug effects / Q000378:metabolism; D016193:G1 Phase / Q000187:drug effects; D019012:Integrin beta1 / Q000378:metabolism; D051379:Mice; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D017469:Receptors, Fibronectin / Q000378:metabolism; D025521:Tumor Suppressor Proteins
chemical_list: D017304:Annexin A5; D015820:Cadherins; C493961:Cdkn1b protein, mouse; D018797:Cell Cycle Proteins; D019012:Integrin beta1; D008869:Microtubule-Associated Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D017469:Receptors, Fibronectin; D025521:Tumor Suppressor Proteins; D050760:Cyclin-Dependent Kinase Inhibitor p27; D004121:Dimethyl Sulfoxide