Apoptosis induced by etoposide in small-cell lung cancer cell lines.
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.
Okamoto-Kubo
S
S
Pharmacology Division, National Cancer Center Research Institute, Tokyo, Japan.
Nishio
K
K
Heike
Y
Y
Yoshida
M
M
Ohmori
T
T
Saijo
N
N
D017209:Apoptosis / Q000187:drug effects*; D018288:Carcinoma, Small Cell / Q000188:drug therapy* / Q000201:enzymology / Q000235:genetics / Q000473:pathology; D004273:DNA, Neoplasm / Q000187:drug effects; D004720:Endonucleases / Q000187:drug effects; D005047:Etoposide / Q000494:pharmacology*; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000201:enzymology / Q000235:genetics / Q000473:pathology; D014407:Tumor Cells, Cultured
D004273:DNA, Neoplasm; D005047:Etoposide; D004720:Endonucleases