Phosphatidylethanolamine biosynthesis in rat mammary carcinoma cells that require and do not require ethanolamine for proliferation.
Phosphatidylethanolamine biosynthesis in rat mammary carcinoma cells that require and do not require ethanolamine for proliferation.
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DOI：
10.1016/s0021-9258(18)45539-1
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发表时间：
1987-05
期刊：
影响因子：
--
通讯作者：
T. Kano‐Sueoka;D. King
中科院分区：
文献类型：
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作者：
T. Kano‐Sueoka;D. King
上皮细胞及其转化衍生物需要乙醇胺才能在确定的培养基中正常生长。当这些细胞在没有乙醇胺的情况下培养时，细胞磷脂酰乙醇胺的数量大大减少。采用一组对乙醇胺有反应（64-24细胞）和无反应（22-1细胞）的大鼠乳腺癌细胞系，研究了乙醇胺反应的生化机制。磷脂的生物合成和代谢，特别是那些涉及磷脂酰乙醇胺，因此比较了两种类型的细胞。64-24细胞中[3H]丝氨酸掺入磷脂酰丝氨酸和磷脂酰乙醇胺的比例分别为22-1细胞的60%和37%。然而，这些细胞系的磷脂酰丝氨酸脱羧酶活性几乎相同。当这些细胞在[32P]磷脂酰胆碱和[32P]磷脂酰乙醇胺中培养时，与22-1细胞相比，64-24细胞从放射性磷脂酰乙醇胺中积累32P标记的磷脂酰丝氨酸的速度大大降低，尽管两种细胞系从放射性磷脂酰胆碱中合成磷脂酰丝氨酸和磷脂酰乙醇胺的速度相似。64-24细胞对放射性磷脂酰乙醇胺中磷脂酰胆碱的标记率也降低，但差异没有磷脂酰丝氨酸大。在64-24细胞中，32P掺入磷脂酰乙醇胺与培养基中乙醇胺的浓度相关，而在22-1细胞中，32P掺入不受乙醇胺的影响。cdp -乙醇胺途径酶活性在两种细胞系间无显著差异。磷脂酰乙醇胺的降解速率在这些细胞系中也相似。这些结果表明，64-24细胞（可能还有其他上皮细胞）对乙醇胺的反应性是由于利用磷脂酰乙醇胺的碱基交换活性有限，合成磷脂酰丝氨酸的能力有限。
Epithelial cells and some of their transformed derivatives require ethanolamine to grow normally in defined culture medium. When these cells are cultured without ethanolamine, the amount of cellular phosphatidylethanolamine is considerably reduced. Using a set of rat mammary carcinoma cell lines whose growth is responsive (64-24 cells) and not responsive (22-1 cells) to ethanolamine, the biochemical mechanism of ethanolamine responsiveness was investigated. The biosynthesis and metabolism of phospholipid, particularly of those involving phosphatidylethanolamine, were thus compared between the two types of cells. The incorporation of [3H]serine into phosphatidylserine and phosphatidylethanolamine in 64-24 cells was 60 and 37%, respectively, of those in 22-1 cells. However, the activity of phosphatidylserine decarboxylase was virtually the same in these cell lines. When these cells were cultured in the presence of [32P]phosphatidylcholine and [32P]phosphatidylethanolamine, the rate of accumulation of 32P-labeled phosphatidylserine from the radioactive phosphatidylethanolamine was considerably reduced in 64-24 cells compared to that in 22-1 cells, although the rate of synthesis of phosphatidylserine and phosphatidylethanolamine from the radioactive phosphatidylcholine was similar between the two cell lines. The rate of labeling phosphatidylcholine from the radioactive phosphatidylethanolamine was also reduced in 64-24 cells, although the difference was not as great as that of phosphatidylserine. Incorporation of 32P into phosphatidylethanolamine was correlated with the concentration of ethanolamine in the culture medium in 64-24 cells, whereas in 22-1 cells the incorporation was not influenced by ethanolamine. Enzyme activities of the CDP-ethanolamine pathway were not significantly different between the two cell lines. The rate of degradation of phosphatidylethanolamine was also similar in these cell lines. These results show that ethanolamine responsiveness of 64-24 cells, and probably other epithelial cells, is due to a limited ability to synthesize phosphatidylserine resulting from a limited base-exchange activity utilizing phosphatidylethanolamine.