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.