Homma M, Homma Y
Dept. of Hygiene and Oncology, Tokyo Medical and Dental University School of Medicine.
Gan To Kagaku Ryoho. 1997 Jan;24(2):156-63.
We analyzed the effect of PLC inhibitor (PCI) peptides in their growth and cell cycle. N-Myristoylated PCI peptide, myr-PCI, originally developed based on the PCI sequence of PLC-gamma 2, inhibited activity of purified PLC isoforms in vitro. When myr-PCI was added to KMS-4 and KMS-8 cells, both derived from familial adenomatous polyposis patients, it suppressed the production of inositol trisphosphate, DNA synthesis, and cell growth, all of which were induced by serum in both KMS 4 and KMS 8 cells. Flow cytometry analysis with propidium iodide labelling revealed marked decreases in the percentage of KMS 8 cells in S phase and increases in G0, G1 by the addition of myr PCI. These results indicate that the activation of PLC is essential for growth and transformed properties of these colorectal carcinoma cells, and also that PLC inhibitors could be an anti-tumor drug for some cases.
我们分析了磷脂酶C抑制剂（PCI）肽对其生长和细胞周期的影响。N-肉豆蔻酰化PCI肽，即myr-PCI，最初是基于磷脂酶Cγ2的PCI序列开发的，在体外可抑制纯化的磷脂酶C同工型的活性。当将myr-PCI添加到均源自家族性腺瘤性息肉病患者的KMS-4和KMS-8细胞中时，它抑制了肌醇三磷酸的产生、DNA合成以及细胞生长，而血清在KMS-4和KMS-8细胞中均可诱导这些过程。用碘化丙啶标记进行的流式细胞术分析显示，添加myr-PCI后，KMS-8细胞S期的百分比显著降低，G0、G1期的百分比增加。这些结果表明，磷脂酶C的激活对于这些结肠癌细胞的生长和转化特性至关重要，并且磷脂酶C抑制剂在某些情况下可能是一种抗肿瘤药物。
