Morphological reversion of sis-transformed NIH3T3 cells by trichostatin A.
Trichostatin A (TSA) induced the normal and flat phenotype of sis-transformed NIH3T3 cells at quite a low concentration of 1 ng/ml. Although morphological changes were found in other oncogene-transformed cells, they were not the same as those seen for the sis-transformed cells. Almost complete reversion into the flat phenotype was seen at 6 h after administration of the compound, suggesting that the morphological change was caused not merely by selection of TSA-resistant cells of the flat phenotype. The effect of TSA was reversible when the cell culture was incubated after its removal. Synthesis of sis-mRNA did not decrease with the treatment of TSA at a concentration sufficient to reverse the transformed morphology. Cycloheximide abolished the activity of TSA, showing that TSA required new protein synthesis to express its activity.
Sugita
K
K
Department of Microbiology, Shionogi Research Laboratories, Shionogi & Co., Ltd., Osaka, Japan.
Koizumi
K
K
Yoshida
H
H
D016475:3T3 Cells / Q000187:drug effects* / Q000473:pathology; D000818:Animals; D002461:Cell Line, Transformed; D003513:Cycloheximide / Q000494:pharmacology; D006877:Hydroxamic Acids / Q000037:antagonists & inhibitors / Q000494:pharmacology; D051379:Mice; D009857:Oncogenes / Q000235:genetics*; D010641:Phenotype; D012333:RNA, Messenger / Q000096:biosynthesis; D014162:Transfection / Q000235:genetics*
D006877:Hydroxamic Acids; D012333:RNA, Messenger; C012589:trichostatin A; D003513:Cycloheximide