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[Cancer Research 52, 168-172, January 1, 1992]
© 1992 American Association for Cancer Research

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Morphological Reversion of sis-transformed NIH3T3 Cells by Trichostatin A

Kenji Sugita1, Kenzo Koizumi and Hiroshi Yoshida

Division of Oncology, Department of Microbiology, Shionogi Research Laboratories, Shionogi & Co., Ltd., 4–12, 5-chome, Sagisu, Fukushima-ku, Osaka 553, Japan

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.

1 To whom requests for reprints should be addressed.

Received 7/30/91. Accepted 10/16/91.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
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Molecular Cancer Research Cancer Prevention Research
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Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1992 by the American Association for Cancer Research.