Yamauchi Y, Nagasawa K, Mayumi T, Horiuchi T, Niho Y
First Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Br J Cancer. 1989 Jul;60(1):15-9. doi: 10.1038/bjc.1989.211.
We attempted to determine whether or not activation of calcium phospholipid-dependent protein kinase C (PKC) is associated with the induction of differentiation by 12-O-tetradecanoylphorbol-13-acetate (TPA) in the human T-lymphoblastic cell line MOLT-3. PKC activities were assayed in MOLT-3 and its five subclones resistant to TPA-induced cell differentiation. The cytosolic PKC activities of TPA-resistant subclones were 36-53% of that of the parental MOLT-3 cells. TPA treatment led to a rapid decrease in PKC activities in the cytosol, together with a concomitant increase in PKC activities in the particulate fraction, in both MOLT-3 and a TPA-resistant subclone. Thus, translocation of PKC from the cytosol to the membrane occurred following treatment with TPA, in both cell lines. However, the amount of PKC translocated from the cytosol to particulate fraction for 60 min in a TPA-resistant subclone was about 20% of that of the parental MOLT-3 cells. These findings suggest that the quantity of cytosolic PKC activity and the extent of translocation may relate to responses to TPA-induced cell differentiation in this T-cell line.
我们试图确定钙磷脂依赖性蛋白激酶C（PKC）的激活是否与12-O-十四烷酰佛波醇-13-乙酸酯（TPA）诱导人T淋巴细胞白血病细胞系MOLT-3分化有关。在MOLT-3及其五个对TPA诱导的细胞分化具有抗性的亚克隆中检测了PKC活性。对TPA有抗性的亚克隆的胞质PKC活性为亲本MOLT-3细胞的36%-53%。在MOLT-3和一个对TPA有抗性的亚克隆中，TPA处理导致胞质中PKC活性迅速下降，同时颗粒部分的PKC活性相应增加。因此，在这两种细胞系中，用TPA处理后PKC从胞质转移到了细胞膜。然而，在一个对TPA有抗性的亚克隆中，60分钟内从胞质转移到颗粒部分的PKC量约为亲本MOLT-3细胞的20%。这些发现表明，胞质PKC活性的量和转移程度可能与该T细胞系中对TPA诱导的细胞分化的反应有关。
