Okamoto-Kubo S, Nishio K, Heike Y, Yoshida M, Ohmori T, Saijo N
Pharmacology Division, National Cancer Center Research Institute, Tokyo, Japan.
Cancer Chemother Pharmacol. 1994;33(5):385-90. doi: 10.1007/BF00686267.
The DNA fragmentation, a parameter of apoptosis, in non-small (NSCLC) and small (SCLC) cell lung cancer cell lines (N231 and PC-9) was evaluated. The DNA fragmentation in SCLC lines, but not in NSCLC lines, was observed in overgrown cells without exposure to anticancer drugs. In etoposide (VP-16)-treated N231 but not PC-9 cells, DNA fragmentation continued to increase up to 42 h, and the increase was dependent on the concentration of VP-16. The endonuclease activity of VP-16-treated N231, but not PC-9, cells required both Ca2+ and Mg2+ for full activity. It was elevated in a time- and concentration-dependent manner. As this activity was not affected by addition of cycloheximide, the activation of the endonuclease activity without protein synthesis may be involved in VP-16-induced cytotoxicity in N231.
对非小细胞肺癌（NSCLC）和小细胞肺癌（SCLC）细胞系（N231和PC-9）中的DNA片段化（细胞凋亡的一个参数）进行了评估。在未接触抗癌药物的过度生长细胞中，观察到SCLC细胞系而非NSCLC细胞系存在DNA片段化。在依托泊苷（VP-16）处理的N231细胞而非PC-9细胞中，DNA片段化持续增加至42小时，且这种增加依赖于VP-16的浓度。VP-16处理的N231细胞而非PC-9细胞的核酸内切酶活性需要Ca2+和Mg2+才能完全发挥作用。它以时间和浓度依赖的方式升高。由于这种活性不受环己酰亚胺添加的影响，核酸内切酶活性在无蛋白质合成情况下的激活可能与VP-16诱导的N231细胞毒性有关。
