Morphology of ras-transformed cells becomes apparently normal again with tyrosine kinase inhibitors without a decrease in the ras-GTP complex

Ho Jeong Kwon, Minoru Yoshida, Kenkoh Muroya, Seisuke Hattori, Eisuke Nishida, Yasuhisa Fukui, Teruhiko Beppu, Sueharu Horinouchi

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Radicicol, an inhibitor of protein-tyrosine kinase, was found to cause morphological reversion of v-Ha-rastransformed NIH3T3 fibroblasts and T24 human urinary bladder carcinoma cells that contain an activated rasmutation. The network of actin stress fihers was restored during the treatment with radicicol. A similar morphological change was observed with another protein-tyrosinc kinase inhibitor, herbimycin A. Radicicol did not cause any changes in the proportion of the active GTP binding form of p21ms or, its subcellular localization. These results rule out the possibility that the morphological reversion by radicicol is due to direct or indirect inhibition of the p21ms function. Cycloheximide and actinomycin D inhibited the morphological change by radicicol, suggesting that the induced transcription of a gene(s) followed by de novo protein synthesis is required for suppression of the transformed phenotype in ras-transformed cells by tyrosine kinase inhibitors.

Original languageEnglish
Pages (from-to)221-228
Number of pages8
JournalJournal of Biochemistry
Volume118
Issue number1
DOIs
Publication statusPublished - 1995 Jan 1

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Guanosine Triphosphate
Protein-Tyrosine Kinases
Dactinomycin
Transcription
Fibroblasts
Cycloheximide
Protein Kinase Inhibitors
Actins
Urinary Bladder
Genes
Cells
monorden
Carcinoma
Phenotype
Proteins

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology

Cite this

Kwon, Ho Jeong ; Yoshida, Minoru ; Muroya, Kenkoh ; Hattori, Seisuke ; Nishida, Eisuke ; Fukui, Yasuhisa ; Beppu, Teruhiko ; Horinouchi, Sueharu. / Morphology of ras-transformed cells becomes apparently normal again with tyrosine kinase inhibitors without a decrease in the ras-GTP complex. In: Journal of Biochemistry. 1995 ; Vol. 118, No. 1. pp. 221-228.
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abstract = "Radicicol, an inhibitor of protein-tyrosine kinase, was found to cause morphological reversion of v-Ha-rastransformed NIH3T3 fibroblasts and T24 human urinary bladder carcinoma cells that contain an activated rasmutation. The network of actin stress fihers was restored during the treatment with radicicol. A similar morphological change was observed with another protein-tyrosinc kinase inhibitor, herbimycin A. Radicicol did not cause any changes in the proportion of the active GTP binding form of p21ms or, its subcellular localization. These results rule out the possibility that the morphological reversion by radicicol is due to direct or indirect inhibition of the p21ms function. Cycloheximide and actinomycin D inhibited the morphological change by radicicol, suggesting that the induced transcription of a gene(s) followed by de novo protein synthesis is required for suppression of the transformed phenotype in ras-transformed cells by tyrosine kinase inhibitors.",
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Morphology of ras-transformed cells becomes apparently normal again with tyrosine kinase inhibitors without a decrease in the ras-GTP complex. / Kwon, Ho Jeong; Yoshida, Minoru; Muroya, Kenkoh; Hattori, Seisuke; Nishida, Eisuke; Fukui, Yasuhisa; Beppu, Teruhiko; Horinouchi, Sueharu.

In: Journal of Biochemistry, Vol. 118, No. 1, 01.01.1995, p. 221-228.

Research output: Contribution to journalArticle

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AU - Kwon, Ho Jeong

AU - Yoshida, Minoru

AU - Muroya, Kenkoh

AU - Hattori, Seisuke

AU - Nishida, Eisuke

AU - Fukui, Yasuhisa

AU - Beppu, Teruhiko

AU - Horinouchi, Sueharu

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AB - Radicicol, an inhibitor of protein-tyrosine kinase, was found to cause morphological reversion of v-Ha-rastransformed NIH3T3 fibroblasts and T24 human urinary bladder carcinoma cells that contain an activated rasmutation. The network of actin stress fihers was restored during the treatment with radicicol. A similar morphological change was observed with another protein-tyrosinc kinase inhibitor, herbimycin A. Radicicol did not cause any changes in the proportion of the active GTP binding form of p21ms or, its subcellular localization. These results rule out the possibility that the morphological reversion by radicicol is due to direct or indirect inhibition of the p21ms function. Cycloheximide and actinomycin D inhibited the morphological change by radicicol, suggesting that the induced transcription of a gene(s) followed by de novo protein synthesis is required for suppression of the transformed phenotype in ras-transformed cells by tyrosine kinase inhibitors.

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