Lack of correlation between effects of tumor promoter TPA on plasminogen activator production, phosphatidyl choline synthesis, and hexose transport in mammalian cell culture systems.
Lack of correlation between effects of tumor promoter TPA on plasminogen activator production, phosphatidyl choline synthesis, and hexose transport in mammalian cell culture systems.
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在哺乳动物细胞培养系统中，肿瘤启动子 TPA 对纤溶酶原激活剂产生、磷脂酰胆碱合成和己糖转运的影响之间缺乏相关性。
DOI：
10.1002/jcp.1041040114
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发表时间：
1980
影响因子：
5.6
通讯作者：
Estensen,RD
中科院分区：
文献类型：
--
作者：
Plagemann,PG;Estensen,RD
本文研究了促癌剂12-0-十四酰佛波酯(TPA)对小鼠L、小鼠P388白血病、人HeLa和中国仓鼠卵巢细胞，以及小鼠肾、小鼠3T3、小鼠3T6和小鼠P388D1巨噬细胞单层培养中纤溶酶原激活剂的产生、己糖转运和代谢以及胆碱掺入酸溶池和磷脂酰胆碱的影响。BHK、3T3、P388D_1和P388细胞组分产生纤溶酶原激活剂，而其他细胞系则无明显产生。TPA仅能诱导或刺激P388细胞产生纤溶酶原激活剂(100 ng/mlTPA可使其增加10~20倍)。另一方面，TPA只在HeLa细胞中刺激磷脂酰胆碱的合成，而用3-0-甲基-D-葡萄糖测得的己糖转运仅在3T3和P388D1细胞以及人淋巴细胞中被刺激。己糖转运的刺激比纤溶酶原激活剂的诱导发生得更快，似乎是细胞对TPA处理的有丝分裂反应的一部分。对脱氧葡萄糖摄取的刺激作用同样仅限于3T3和P388D1细胞。在P388和P388D1细胞中，脱氧葡萄糖的碳1发生了显著的脱羧基，而在Novikoff细胞中则没有，而且发生的任何脱羧基都不被TPA刺激。结果表明，细胞对TPA的各种反应是不相关的，相互独立地发生。生化反应的时间进程也有显著差异。
We have investigated the effects of the tumor promoter 12‐0‐tetradecanoyl‐phorbol‐13‐acetate (TPA) on plasminogen activator production, hexose transport and metabolism, and the incorporation of choline into the acid soluble pool and into phosphatidylcholine in suspension cultures of mouse L, mouse P388 leukemia, human HeLa, and Chinese hamster ovary cells, and in monolayer cultures of baby hamster kidney (BHK), mouse 3T3, mouse 3T6, and mouse P388D1 macrophage‐like cells. BHK, 3T3, P388D1, and P388 cells produced plasminogen activator constitutively, but no significant production was observed in the other cell lines. Plasminogen activator production was induced or stimulated by TPA only in P388 cells (10‐ to 20‐fold by 100 ng TPA/ml). On the other hand, phosphatidylcholine synthesis was stimulated by TPA only in HeLa cells, and hexose transport, as measured with 3‐0‐methyl‐D‐glucose, only in 3T3 and P388D1 cells, as well as in human lymphocytes. The stimulation of hexose transport occurred more rapidly than the induction of plasminogen activator production and seemed to be part of the mitogenic response of cells to TPA treatment. A stimulation of deoxyglucose uptake was similarly limited to 3T3 and P388D1 cells. A significant decarboxylation of carbon 1 of deoxyglucose occurred in P388 and P388D1 cells, but not in Novikoff cells, and any decarboxylation that occurred was not stimulated by TPA. The results indicate that the various investigated responses of cells to TPA are unrelated and occur independent of each other. The time courses of the biochemical responses also differ significantly.