Nagasawa K, Howatson A, Mak T W
J Cell Physiol. 1981 Oct;109(1):181-92. doi: 10.1002/jcp.1041090120.
The process of induction of human malignant T-lymphoblastic cell line MOLT-3 by the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) was examined. It was found that the induction process by TPA, which included increase in cells with receptors to sheep red blood cells (E--rosette positive--E+) and decrease in the levels of the marker enzyme terminal deoxynucleotidyl transferase (TdT) was not affected by the presence of DNA synthesis inhibitor arabinofuranosylcytosine (Ara-C). The exposure time to TPA required to elicit these changes was found to be short, in the order of 1 hour or less. The kinetics of the increased in E+ cells, decrease in the levels of TdT in these cells, or decrease in the ability to proliferate as measured by colony formation were similar with exposure to TPA for 1, 6, 24, or 96 hours. We have examined the effect of antitumor promoter compounds on their ability to block induction of MOLT-3 cells by TPA. Results indicated that none of these compounds, dexamethasone, antipain, retinoic acid, and L-1-tosylamide-2-phenylethylchloromethyl ketone (TPCK), was effective in reducing the number of E+ cells induced by TPA. Examination of three other leukemic T-cell lines indicated that, in addition to MOLT-3, the leukemic T-cell line Jurkat also responded to TPA, whereas two other leukemic T-cells lines CCRF-CEM and CCRF-HSB-2 did not. Certain physical and morphological changes were also observed after stimulation of MOLT-3 cells and Jurkat cells by TPA. We found that, following the addition of TPA, the cell volumes of MOLT-3 cells decreased from an average of 1150 micrometers3 to about 500 micrometers3, whereas those of Jurkat were reduced to about 700 micrometers3 from 1100 micrometers3. Electron microscopic studies of these lymphoblasts also revealed that after treatment with TPA the induced cells were generally smaller in size with increase in the density of the nuclear materials and condensation of the chromatin structures.
研究了佛波酯12 - O -十四烷酰佛波醇-13 -乙酸酯（TPA）诱导人恶性T淋巴细胞系MOLT - 3的过程。发现TPA的诱导过程，包括对绵羊红细胞有受体的细胞（E - 玫瑰花结阳性 - E +）数量增加以及标记酶末端脱氧核苷酸转移酶（TdT）水平降低，不受DNA合成抑制剂阿糖胞苷（Ara - C）存在的影响。引发这些变化所需的TPA暴露时间很短，约为1小时或更短。E +细胞增加、这些细胞中TdT水平降低或通过集落形成测量的增殖能力降低的动力学，在暴露于TPA 1、6、24或96小时时相似。我们研究了抗肿瘤促进剂化合物对其阻断TPA诱导MOLT - 3细胞能力的影响。结果表明，这些化合物，地塞米松、抑肽酶、视黄酸和L - 1 -甲苯磺酰氨基-2 -苯乙基氯甲基酮（TPCK），均不能有效减少TPA诱导的E +细胞数量。对其他三种白血病T细胞系的研究表明，除了MOLT - 3外，白血病T细胞系Jurkat也对TPA有反应，而另外两种白血病T细胞系CCRF - CEM和CCRF - HSB - 2则无反应。在TPA刺激MOLT - 3细胞和Jurkat细胞后，还观察到某些物理和形态学变化。我们发现，加入TPA后，MOLT - 3细胞的体积从平均1150立方微米降至约500立方微米，而Jurkat细胞的体积从1100立方微米降至约700立方微米。对这些淋巴母细胞的电子显微镜研究还显示，用TPA处理后，诱导的细胞通常尺寸较小，核物质密度增加，染色质结构凝聚。
