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.
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.
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猿病毒 40、多瘤病毒、EJ-ras 或 v-myc 癌基因对乙醇胺反应性乳腺细胞转化为乙醇胺无反应性细胞的转化不足。
DOI：
10.1128/jvi.62.9.3201-3209.1988
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发表时间：
1988
影响因子：
5.4
通讯作者：
King,DM
中科院分区：
文献类型：
--
作者：
Kano-Sueoka,T;King,DM
正常乳腺上皮细胞（对乙醇胺有反应）需要乙醇胺使其能够在确定的培养基中生长，因为它们不能从头合成足够数量的磷脂酰乙醇胺。保留正常组织特性的乳腺肿瘤细胞也可能对乙醇胺有反应，而去分化、高度致瘤性的乳腺肿瘤细胞对乙醇胺无反应。无反应的肿瘤细胞能够合成必要数量的磷脂酰乙醇胺来维持生长。因此，恶性肿瘤的进展似乎将对乙醇胺有反应的乳腺细胞转化为对乙醇胺无反应的细胞。为了证明上述假设并了解恶性转化过程中转化的机制，将典型的乙醇胺反应性的乳腺肿瘤细胞系64-24转染类人猿病毒40、多瘤病毒、EJ-ras或v-myc癌基因，并检测所产生的转染物对乙醇胺的生长反应。许多转基因表现出典型的转化表型；然而，没有一种转染物转化为乙醇胺无反应细胞。一些SV40和多瘤病毒转化体能够在没有乙醇胺的情况下生长，尽管它们在乙醇胺存在的情况下生长得更好，这与典型的乙醇胺无反应细胞不同。这些细胞可以在没有乙醇胺的情况下生长，即使它们的膜磷脂缺乏磷脂酰乙醇胺。目前的研究表明，在64-24个细胞中，四种癌基因中的任何一种的表达都不足以使乙醇胺反应细胞转化为非反应细胞。
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.