Mechanism of apoptosis induced by cisplatin and VP-16 in PANC-1 cells.
Jeon Uk Lee, Ryo Hosotani, Michihiko Wada, Ryuichiro Doi, T Kosiba, Kazuma Fujimoto, Yasunori Miyamoto, Chihiro Mori, Noriko Nakamura, Kohei Shiota, M Imamura
Abstract
Jeon Uk Lee, Ryo Hosotani, Michihiko Wada, Ryuichiro Doi, T Kosiba, Kazuma Fujimoto, Yasunori Miyamoto, Chihiro Mori, Noriko Nakamura, Kohei Shiota, M Imamura
Abstract
Cisplatin and VP-16 were used to study the induction of apoptosis in Panc-1 cells. Cisplatin and VP-16 inhibited the growth of Panc-1 cells. After 2 hours exposure to cisplatin or VP-16, attached and detached cells were subjected to TUNEL staining to calculate the ratio of apoptosis. In detached cells TUNEL positive ratios increased in a time- and dose-dependent manner. In Western blotting, Bax expression was obviously up-regulated, but Bcl-2 remained almost constant. The results suggested that in Panc-1 cells cisplatin and VP-16 induced apoptotic cell death which was mediated through the interaction of Bax expression in the presence of mutated p53.
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Cisplatin and VP-16 were used to study the induction of apoptosis in Panc-1 cells. Cisplatin and VP-16 inhibited the growth of Panc-1 cells. After 2 hours exposure to cisplatin or VP-16, attached and detached cells were subjected to TUNEL staining to calculate the ratio of apoptosis. In detached cells TUNEL positive ratios increased in a time- and dose-dependent manner. In Western blotting, Bax expression was obviously up-regulated, but Bcl-2 remained almost constant. The results suggested that in Panc-1 cells cisplatin and VP-16 induced apoptotic cell death which was mediated through the interaction of Bax expression in the presence of mutated p53.
Key concepts: Cisplatin, Apoptosis, TUNEL assay, Blot, Programmed cell death, Molecular biology, Chemistry, Biology