Overexpression of protein kinase C beta 1 is not sufficient to induce factor independence in the interleukin-3-dependent myeloid cell line FDC-P1.
Overexpression of protein kinase C beta 1 is not sufficient to induce factor independence in the interleukin-3-dependent myeloid cell line FDC-P1.
复制标题
蛋白激酶 C beta 1 的过度表达不足以诱导白细胞介素 3 依赖性骨髓细胞系 FDC-P1 中的因子独立性。
作者：
A. Kraft;F. Wagner;G. Housey
为了检查蛋白激酶C（PKC）的过表达是否足以使造血细胞实现因子非依赖性生长，我们使用重组逆转录病毒表达载体系统将编码PKC基因β 1亚型的cDNA导入IL-3依赖性细胞FDC-P1。产生的细胞系含有高达24倍的PKC活性增加。对这些细胞系的分析表明，PKC的激活在IL-3介导的生长控制中不起重要作用，如以下所证明的：（1）IL-3加入到过表达细胞系中不引起形态学变化，而PKC激活剂刺激细胞聚集;（2）PKC激活剂不能刺激PKC正常或升高的早期传代FDC-P1细胞生长;和（3）向这些细胞中加入佛波醇酯或苔藓抑素1显著降低了PKC的水平，而不影响这些细胞在IL-3中生长的能力。因此，我们认为IL-3介导的生长是通过PKC以外的途径发生的。
To examine whether overexpression of protein kinase C (PKC) is sufficient to allow for factor-independent growth in hematopoietic cells, we used a recombinant retroviral expression vector system to introduce a cDNA encoding the beta 1 isoform of the PKC gene into IL-3-dependent cells FDC-P1. Cell lines were generated which contained up to 24-fold increases in PKC activity. Analysis of these cell lines demonstrated that PKC activation does not play a significant role in IL-3-mediated growth control, as evidenced by the following: (1) IL-3 addition to either overexpressor cell lines did not induce morphologic changes whereas activators of PKC stimulated cellular clumping; (2) early passage FDC-P1 cells, either carrying normal or elevated levels of PKC, were not stimulated to grow by activators of PKC; and (3) addition of phorbol esters or bryostatin 1 to these cells markedly decreased the levels of PKC without affecting the ability of these cells to grow in IL-3. Therefore, we suggest that IL-3 mediated growth occurs through pathways other than involving PKC.