title: Insufficiency of transformation by simian virus 40, polyomavirus, EJ-ras, or v-myc oncogenes for conversion of ethanolamine-responsive mammary cells to ethanolamine-nonresponsive cells.
abstract: Normal mammary epithelial cells (ethanolamine responsive) require ethanolamine to enable them to grow in defined culture medium because they cannot synthesize de novo a sufficient amount of phosphatidylethanolamine. Mammary tumor cells which retain properties of the normal tissue are also likely to be ethanolamine responsive, whereas dedifferentiated, highly tumorigenic mammary tumor cells are ethanolamine nonresponsive. The nonresponsive tumor cells are able to synthesize the necessary amount of phosphatidylethanolamine to sustain growth. Therefore, the progression of malignancy seems to convert ethanolamine-responsive mammary cells to ethanolamine-nonresponsive ones. In an attempt to prove the above assumption and to understand the mechanism responsible for the conversion during the progression of malignant transformation, mammary tumor cell line 64-24, which is typically ethanolamine responsive, was transfected with simian virus 40, polyomavirus, EJ-ras, or v-myc oncogenes, and the resulting transfectants were examined for their growth response to ethanolamine. Many of the transfectants exhibited typical transformed phenotypes; however, none of the transfectants converted to ethanolamine-nonresponsive cells. Some of the SV40 and polyomavirus transformants were able to grow in the absence of ethanolamine, although they grew better in the presence of ethanolamine, unlike typical ethanolamine-nonresponsive cells. These cells could grow in the absence of ethanolamine, even though their membrane phospholipid was phosphatidylethanolamine deficient. The present study indicates that the expression of any one of the four oncogenes tested, which allows the cells to exhibit transformed phenotypes in 64-24 cells, is not sufficient for the conversion of ethanolamine-responsive cells to -nonresponsive cells.
authors.affiliation: Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder 80309-0347.
authors.forename: T
authors.initials: T
authors.lastname: Kano-Sueoka
authors.forename: D M
authors.initials: DM
authors.lastname: King
mesh_terms: D000818:Animals; D000952:Antigens, Polyomavirus Transforming / Q000235:genetics; D002455:Cell Division / Q000187:drug effects*; D002471:Cell Transformation, Neoplastic; D002472:Cell Transformation, Viral; D004279:DNA, Viral / Q000235:genetics; D004983:Ethanolamines / Q000494:pharmacology*; D005260:Female; D005814:Genes, Viral; D008325:Mammary Neoplasms, Experimental; D009857:Oncogenes; D010957:Plasmids; D011120:Polyomavirus / Q000235:genetics / Q000276:immunology; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis / Q000235:genetics; D016283:Proto-Oncogene Proteins p21(ras); D051381:Rats; D013539:Simian virus 40 / Q000235:genetics / Q000276:immunology; D014162:Transfection; D014407:Tumor Cells, Cultured
chemical_list: D000952:Antigens, Polyomavirus Transforming; D004279:DNA, Viral; D004983:Ethanolamines; D011518:Proto-Oncogene Proteins; D016283:Proto-Oncogene Proteins p21(ras)