An exogenous cdk inhibitor, butyrolactone-I, induces apoptosis with increased Bax/Bcl-2 ratio in p53-mutated pancreatic cancer cells

Michihiko Wada, Ryo Hosotani, Jeon Uk Lee, Ryuichiro Doi, Takatomo Koshiba, Koji Fujimoto, Yoshiharu Miyamoto, Shoichiro Tsuji, Sanae Nakajima, Akira Okuyama, Masayuki Imamura

研究成果: Article

23 引用 (Scopus)

抄録

We investigated the effects of an exogenous cdk inhibitor, butyrolactone-I, on cell growth inhibition, apoptosis induction, and the regulation of apoptosis in pancreatic cancer cells with mutated p53. Cell growth was dose-dependently inhibited by Butyrolactone-I in PANC-1 and AsPC-1 cells. Phosphorylation of pRb and Cyclin A expression were significantly inhibited in Butyrolactone-I-treated cells. Apoptotic cell death was detected by both Hoechst staining and TUNEL assay. In butyrolactone-I-treated PANC-1 cells, expression of p53 protein was unchanged, but Bax expression was slightly up-regulated and Bcl-2 expression was predominantly down-regulated. Bax/Bcl-2 ratio reached 9.6-fold increase compared to the control at the maximum. The time course of changes in Bax/Bcl-2 ratio was similar to that in the TUNEL-positive ratio. These data, suggest that dynamic changes of the Bax/Bcl-2 ratio might be important in determining point of apoptosis induction in pancreatic cancer cells with p53 mutation.

元の言語English
ページ(範囲)2559-2566
ページ数8
ジャーナルAnticancer research
18
発行部数4 A
出版物ステータスPublished - 01-07-1998

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Pancreatic Neoplasms
Apoptosis
In Situ Nick-End Labeling
Cyclin A
Growth
butyrolactone I
Cell Death
Phosphorylation
Staining and Labeling
Mutation
Proteins

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

これを引用

Wada, M., Hosotani, R., Lee, J. U., Doi, R., Koshiba, T., Fujimoto, K., ... Imamura, M. (1998). An exogenous cdk inhibitor, butyrolactone-I, induces apoptosis with increased Bax/Bcl-2 ratio in p53-mutated pancreatic cancer cells. Anticancer research, 18(4 A), 2559-2566.
Wada, Michihiko ; Hosotani, Ryo ; Lee, Jeon Uk ; Doi, Ryuichiro ; Koshiba, Takatomo ; Fujimoto, Koji ; Miyamoto, Yoshiharu ; Tsuji, Shoichiro ; Nakajima, Sanae ; Okuyama, Akira ; Imamura, Masayuki. / An exogenous cdk inhibitor, butyrolactone-I, induces apoptosis with increased Bax/Bcl-2 ratio in p53-mutated pancreatic cancer cells. :: Anticancer research. 1998 ; 巻 18, 番号 4 A. pp. 2559-2566.
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title = "An exogenous cdk inhibitor, butyrolactone-I, induces apoptosis with increased Bax/Bcl-2 ratio in p53-mutated pancreatic cancer cells",
abstract = "We investigated the effects of an exogenous cdk inhibitor, butyrolactone-I, on cell growth inhibition, apoptosis induction, and the regulation of apoptosis in pancreatic cancer cells with mutated p53. Cell growth was dose-dependently inhibited by Butyrolactone-I in PANC-1 and AsPC-1 cells. Phosphorylation of pRb and Cyclin A expression were significantly inhibited in Butyrolactone-I-treated cells. Apoptotic cell death was detected by both Hoechst staining and TUNEL assay. In butyrolactone-I-treated PANC-1 cells, expression of p53 protein was unchanged, but Bax expression was slightly up-regulated and Bcl-2 expression was predominantly down-regulated. Bax/Bcl-2 ratio reached 9.6-fold increase compared to the control at the maximum. The time course of changes in Bax/Bcl-2 ratio was similar to that in the TUNEL-positive ratio. These data, suggest that dynamic changes of the Bax/Bcl-2 ratio might be important in determining point of apoptosis induction in pancreatic cancer cells with p53 mutation.",
author = "Michihiko Wada and Ryo Hosotani and Lee, {Jeon Uk} and Ryuichiro Doi and Takatomo Koshiba and Koji Fujimoto and Yoshiharu Miyamoto and Shoichiro Tsuji and Sanae Nakajima and Akira Okuyama and Masayuki Imamura",
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Wada, M, Hosotani, R, Lee, JU, Doi, R, Koshiba, T, Fujimoto, K, Miyamoto, Y, Tsuji, S, Nakajima, S, Okuyama, A & Imamura, M 1998, 'An exogenous cdk inhibitor, butyrolactone-I, induces apoptosis with increased Bax/Bcl-2 ratio in p53-mutated pancreatic cancer cells', Anticancer research, 巻. 18, 番号 4 A, pp. 2559-2566.

An exogenous cdk inhibitor, butyrolactone-I, induces apoptosis with increased Bax/Bcl-2 ratio in p53-mutated pancreatic cancer cells. / Wada, Michihiko; Hosotani, Ryo; Lee, Jeon Uk; Doi, Ryuichiro; Koshiba, Takatomo; Fujimoto, Koji; Miyamoto, Yoshiharu; Tsuji, Shoichiro; Nakajima, Sanae; Okuyama, Akira; Imamura, Masayuki.

:: Anticancer research, 巻 18, 番号 4 A, 01.07.1998, p. 2559-2566.

研究成果: Article

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AU - Wada, Michihiko

AU - Hosotani, Ryo

AU - Lee, Jeon Uk

AU - Doi, Ryuichiro

AU - Koshiba, Takatomo

AU - Fujimoto, Koji

AU - Miyamoto, Yoshiharu

AU - Tsuji, Shoichiro

AU - Nakajima, Sanae

AU - Okuyama, Akira

AU - Imamura, Masayuki

PY - 1998/7/1

Y1 - 1998/7/1

N2 - We investigated the effects of an exogenous cdk inhibitor, butyrolactone-I, on cell growth inhibition, apoptosis induction, and the regulation of apoptosis in pancreatic cancer cells with mutated p53. Cell growth was dose-dependently inhibited by Butyrolactone-I in PANC-1 and AsPC-1 cells. Phosphorylation of pRb and Cyclin A expression were significantly inhibited in Butyrolactone-I-treated cells. Apoptotic cell death was detected by both Hoechst staining and TUNEL assay. In butyrolactone-I-treated PANC-1 cells, expression of p53 protein was unchanged, but Bax expression was slightly up-regulated and Bcl-2 expression was predominantly down-regulated. Bax/Bcl-2 ratio reached 9.6-fold increase compared to the control at the maximum. The time course of changes in Bax/Bcl-2 ratio was similar to that in the TUNEL-positive ratio. These data, suggest that dynamic changes of the Bax/Bcl-2 ratio might be important in determining point of apoptosis induction in pancreatic cancer cells with p53 mutation.

AB - We investigated the effects of an exogenous cdk inhibitor, butyrolactone-I, on cell growth inhibition, apoptosis induction, and the regulation of apoptosis in pancreatic cancer cells with mutated p53. Cell growth was dose-dependently inhibited by Butyrolactone-I in PANC-1 and AsPC-1 cells. Phosphorylation of pRb and Cyclin A expression were significantly inhibited in Butyrolactone-I-treated cells. Apoptotic cell death was detected by both Hoechst staining and TUNEL assay. In butyrolactone-I-treated PANC-1 cells, expression of p53 protein was unchanged, but Bax expression was slightly up-regulated and Bcl-2 expression was predominantly down-regulated. Bax/Bcl-2 ratio reached 9.6-fold increase compared to the control at the maximum. The time course of changes in Bax/Bcl-2 ratio was similar to that in the TUNEL-positive ratio. These data, suggest that dynamic changes of the Bax/Bcl-2 ratio might be important in determining point of apoptosis induction in pancreatic cancer cells with p53 mutation.

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