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Mol. Cells 2002; 14(3): 348-354

Published online January 1, 1970

© The Korean Society for Molecular and Cellular Biology

MAPK Signaling Is Involved in Camptothecin-induced Cell Death

Seongeun Lee, Ho-Soon Lee, Myunginq Baek, Dae-Yeon Lee, Yung-Jue Bang, Hae-Nyun Cho, Yun-Sil Lee, Ji-Hong Ha, Hae-Yeong Kim, Doo-Il Jeong

Abstract

Camptothecin, a topoisomerase I inhibitor, is a well-known anticancer drug. However, its mechanism has not been well studied in human gastric cancer cell lines. Camptothecin induced apoptotic cell death in human gastric cancer cell line AGS. Z-VAD-fmk, pan-caspase inhibitor, blocked apoptotic phenotypes induced by camptothecin suggesting that caspases are involved in camptothecin-induced cell death. An inhibitor of caspase-6 or -8 or -9 did not prevent cell death by camptothecin. Various protease inhibitors failed to prevent camptothecin-induced cell death. These results suggest that only few caspases are involved in camptothecin-induced cell death. Camptothecin induced phosphorylation of ERK1/2, JNK, and p38 MAPK, in a dose and time-dependent manner in AGS. Z-VAD-fmk did not affect MAPK signaling induced by camptothecin suggesting that caspase signaling occurs downstream of MAPK signaling. Blocking of p38 MAPK, but not ERK1/2, resulted in partial inhibition of cell death and PARP cleavage by camptothecin in AGS. Taken together, MAPK signaling is associated with apoptotic cell death by camptothecin.

Keywords MAPK, Camptothecin, Apoptosis, AGS

Article

Research Article

Mol. Cells 2002; 14(3): 348-354

Published online December 31, 2002

Copyright © The Korean Society for Molecular and Cellular Biology.

MAPK Signaling Is Involved in Camptothecin-induced Cell Death

Seongeun Lee, Ho-Soon Lee, Myunginq Baek, Dae-Yeon Lee, Yung-Jue Bang, Hae-Nyun Cho, Yun-Sil Lee, Ji-Hong Ha, Hae-Yeong Kim, Doo-Il Jeong

Abstract

Camptothecin, a topoisomerase I inhibitor, is a well-known anticancer drug. However, its mechanism has not been well studied in human gastric cancer cell lines. Camptothecin induced apoptotic cell death in human gastric cancer cell line AGS. Z-VAD-fmk, pan-caspase inhibitor, blocked apoptotic phenotypes induced by camptothecin suggesting that caspases are involved in camptothecin-induced cell death. An inhibitor of caspase-6 or -8 or -9 did not prevent cell death by camptothecin. Various protease inhibitors failed to prevent camptothecin-induced cell death. These results suggest that only few caspases are involved in camptothecin-induced cell death. Camptothecin induced phosphorylation of ERK1/2, JNK, and p38 MAPK, in a dose and time-dependent manner in AGS. Z-VAD-fmk did not affect MAPK signaling induced by camptothecin suggesting that caspase signaling occurs downstream of MAPK signaling. Blocking of p38 MAPK, but not ERK1/2, resulted in partial inhibition of cell death and PARP cleavage by camptothecin in AGS. Taken together, MAPK signaling is associated with apoptotic cell death by camptothecin.

Keywords: MAPK, Camptothecin, Apoptosis, AGS

Mol. Cells
Nov 30, 2023 Vol.46 No.11, pp. 655~725
COVER PICTURE
Kim et al. (pp. 710-724) demonstrated that a pathogen-derived Ralstonia pseudosolanacearum type III effector RipL delays flowering time and enhances susceptibility to bacterial infection in Arabidopsis thaliana. Shown is the RipL-expressing Arabidopsis plant, which displays general dampening of the transcriptional program during pathogen infection, grown in long-day conditions.

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