| Growth inhibition of oncogene-transformed rat fibroblasts by cocultured normal cells: relevance of metabolic cooperation mediated by gap junctions. | |
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MedLine Citation:
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PMID: 1913656 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We have studied the proliferation of rat 208F cells (a derivative of Rat-1 cells) transformed by activated c-Ha-ras, v-fgr, v-raf, v-fms, or v-src oncogenes during cocultivation with an excess of early passage rat embryonic fibroblasts or immortal 208F cells. The total number and size of foci formed by oncogene-transformed 208F cells were strongly reduced by cocultured normal fibroblasts. The extent of growth suppression of transformed foci appears to be dependent on the type of transforming oncogene and on the type of normal fibroblasts rather than on the extent of gap-junctional communication between transformed and normal cells. Total inhibition of fluorescent dye transfer between normal and transformed cells by the 3 beta-O-hemisuccinate of 18 alpha-glycyrrhetinic acid (18 alpha-carbenoxolone), an inhibitor of gap-junctional communication in human fibroblasts, did not prevent growth inhibition of transformed cells in the cocultivation assay. Since adjacent cells remained electrically coupled in the presence of this inhibitor it is possible that the strongly reduced metabolic cooperation, as indicated by the lack of fluorescent dye transfer, is sufficient for mediating the growth-inhibitory effect of normal fibroblasts. 208F cell-conditioned medium, however, also caused strong growth inhibition of transformed derivatives, suggesting that the effect is in part mediated by release of stable growth inhibitor(s) from 208F cells. |
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Authors:
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W Martin; G Zempel; D Hülser; K Willecke |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Cancer research Volume: 51 ISSN: 0008-5472 ISO Abbreviation: Cancer Res. Publication Date: 1991 Oct |
Date Detail:
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Created Date: 1991-10-29 Completed Date: 1991-10-29 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 2984705R Medline TA: Cancer Res Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 5348-51 Citation Subset: IM |
Affiliation:
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Institut für Genetik (Abt. Molekulargenetik), Universität Bonn, Federal Republic of Germany. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Carbenoxolone / pharmacology Cell Adhesion Cell Communication / drug effects, physiology Cell Division / physiology Cell Line Cell Transformation, Neoplastic / genetics Cells, Cultured Fibroblasts / physiology* Intercellular Junctions / drug effects, physiology* Neoplasms / pathology* Oncogenes Plasmids Rats |
| Chemical | |
Reg. No./Substance:
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5697-56-3/Carbenoxolone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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