Dihydrocytochalasin B disorganizes actin cytoarchitecture and inhibits initiation of DNA synthesis in 3T3 cells.
Dihydrocytochalasin B (H2CB) disrupts the actin structure of Swiss/3T3 mouse fibroblasts and inhibits the ability of serum growth factors to stimulate DNA synthesis in quiescent cultures. Low doses of H2CB (2-10 X 10(-7) M) added to serum-arrested cells reversibly block initiation of DNA synthesis by serum; by epidermal growth factor and insulin; or by epidermal growth factor, fibroblast growth factor and insulin. H2CB is effective only when added to cells within 8-10 hr after stimulation. Low doses of H2CB cause cell rounding and a loss of actin microfilament bundles, but they do not interfere with glucose or thymidine transport. These results suggest that stimulation of 3T3 cells involves at least one obligatory actin-mediated step. Transformed cells appear to obviate this step, for H2CB does not inhibit the entry into S phase of SV40-transformed or Moloney murine sarcoma virus-transformed 3T3 cells synchronized by mitotic shake-off.
D000199:Actins; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D001769:Blood; D002460:Cell Line; D002472:Cell Transformation, Viral; D003571:Cytochalasin B / Q000031:analogs & derivatives* / Q000494:pharmacology; D003599:Cytoskeleton / Q000187:drug effects*; D004247:DNA / Q000096:biosynthesis*; D004305:Dose-Response Relationship, Drug; D004815:Epidermal Growth Factor / Q000494:pharmacology; D005346:Fibroblast Growth Factors; D005947:Glucose / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology; D046911:Macromolecular Substances; D051379:Mice; D010455:Peptides / Q000494:pharmacology; D013936:Thymidine / Q000378:metabolism
D000199:Actins; D007328:Insulin; D046911:Macromolecular Substances; D010455:Peptides; C024794:dihydrocytochalasin B; D003571:Cytochalasin B; D005346:Fibroblast Growth Factors; D004815:Epidermal Growth Factor; D004247:DNA; D005947:Glucose; D013936:Thymidine