Nuclear interaction of Smac/DIABLO with Survivin at G2/M arrest prompts docetaxel-induced apoptosis in DU145 prostate cancer cells

Ji Young Kim; Jin Yong Chung; Seung Gee Lee; Yoon Jae Kim; Ji Eun Park; Ki Soo Yoo; Young Hyun Yoo; Young Chul Park; Byeong Gee Kim; Jong Min Kim

doi:10.1016/j.bbrc.2006.09.143

Nuclear interaction of Smac/DIABLO with Survivin at G2/M arrest prompts docetaxel-induced apoptosis in DU145 prostate cancer cells

Ji Young Kim, Jin Yong Chung, Seung Gee Lee, Yoon Jae Kim, Ji Eun Park, Ki Soo Yoo, Young Hyun Yoo, Young Chul Park, Byeong Gee Kim, Jong Min Kim

Research output: Contribution to journal › Article › peer-review

Abstract

Smac/DIABLO is released by mitochondria in response to apoptotic stimuli and is thought to antagonize the function of inhibitors of apoptosis proteins. Recently, it has been shown that, like XIAP, Survivin can potentially interact with Smac/DIABLO. However, the precise mechanisms and cellular location of their action have not been determined. We report for the first time that Smac/DIABLO translocates to the nucleus and is colocalized with Survivin at mitotic spindles during apoptosis resulting from G2/M arrest due to docetaxel treatment of DU145 prostate cancer cells. Our data demonstrate that the nuclear interaction of Smac/DIABLO with Survivin is an important step for suppressing the anti-apoptotic function of Survivin in Doc-induced apoptosis. This suggests that the balance between cellular Smac/DIABLO and Survivin levels could be critical for cellular destiny in taxane-treated cancer cells.

Original language	English (US)
Pages (from-to)	949-954
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	350
Issue number	4
DOIs	https://doi.org/10.1016/j.bbrc.2006.09.143
State	Published - Dec 1 2006
Externally published	Yes

Keywords

Apoptosis
G2/M arrest
Mitotic apparatus
Prostate cancer
Smac
Survivin

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1016/j.bbrc.2006.09.143

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Kim, J. Y., Chung, J. Y., Lee, S. G., Kim, Y. J., Park, J. E., Yoo, K. S., Yoo, Y. H., Park, Y. C., Kim, B. G., & Kim, J. M. (2006). Nuclear interaction of Smac/DIABLO with Survivin at G2/M arrest prompts docetaxel-induced apoptosis in DU145 prostate cancer cells. Biochemical and Biophysical Research Communications, 350(4), 949-954. https://doi.org/10.1016/j.bbrc.2006.09.143

Nuclear interaction of Smac/DIABLO with Survivin at G2/M arrest prompts docetaxel-induced apoptosis in DU145 prostate cancer cells. / Kim, Ji Young; Chung, Jin Yong; Lee, Seung Gee; Kim, Yoon Jae; Park, Ji Eun; Yoo, Ki Soo; Yoo, Young Hyun; Park, Young Chul; Kim, Byeong Gee; Kim, Jong Min.

In: Biochemical and Biophysical Research Communications, Vol. 350, No. 4, 01.12.2006, p. 949-954.

Research output: Contribution to journal › Article › peer-review

Kim, Ji Young ; Chung, Jin Yong ; Lee, Seung Gee ; Kim, Yoon Jae ; Park, Ji Eun ; Yoo, Ki Soo ; Yoo, Young Hyun ; Park, Young Chul ; Kim, Byeong Gee ; Kim, Jong Min. / Nuclear interaction of Smac/DIABLO with Survivin at G2/M arrest prompts docetaxel-induced apoptosis in DU145 prostate cancer cells. In: Biochemical and Biophysical Research Communications. 2006 ; Vol. 350, No. 4. pp. 949-954.

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title = "Nuclear interaction of Smac/DIABLO with Survivin at G2/M arrest prompts docetaxel-induced apoptosis in DU145 prostate cancer cells",

abstract = "Smac/DIABLO is released by mitochondria in response to apoptotic stimuli and is thought to antagonize the function of inhibitors of apoptosis proteins. Recently, it has been shown that, like XIAP, Survivin can potentially interact with Smac/DIABLO. However, the precise mechanisms and cellular location of their action have not been determined. We report for the first time that Smac/DIABLO translocates to the nucleus and is colocalized with Survivin at mitotic spindles during apoptosis resulting from G2/M arrest due to docetaxel treatment of DU145 prostate cancer cells. Our data demonstrate that the nuclear interaction of Smac/DIABLO with Survivin is an important step for suppressing the anti-apoptotic function of Survivin in Doc-induced apoptosis. This suggests that the balance between cellular Smac/DIABLO and Survivin levels could be critical for cellular destiny in taxane-treated cancer cells.",

keywords = "Apoptosis, G2/M arrest, Mitotic apparatus, Prostate cancer, Smac, Survivin",

author = "Kim, {Ji Young} and Chung, {Jin Yong} and Lee, {Seung Gee} and Kim, {Yoon Jae} and Park, {Ji Eun} and Yoo, {Ki Soo} and Yoo, {Young Hyun} and Park, {Young Chul} and Kim, {Byeong Gee} and Kim, {Jong Min}",

note = "Funding Information: This work was supported by grants from Korea Research Foundation Grant (2004-005-E00006).",

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doi = "10.1016/j.bbrc.2006.09.143",

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AU - Chung, Jin Yong

AU - Lee, Seung Gee

AU - Kim, Yoon Jae

AU - Park, Ji Eun

AU - Yoo, Ki Soo

AU - Yoo, Young Hyun

AU - Park, Young Chul

AU - Kim, Byeong Gee

AU - Kim, Jong Min

N1 - Funding Information: This work was supported by grants from Korea Research Foundation Grant (2004-005-E00006).

PY - 2006/12/1

Y1 - 2006/12/1

N2 - Smac/DIABLO is released by mitochondria in response to apoptotic stimuli and is thought to antagonize the function of inhibitors of apoptosis proteins. Recently, it has been shown that, like XIAP, Survivin can potentially interact with Smac/DIABLO. However, the precise mechanisms and cellular location of their action have not been determined. We report for the first time that Smac/DIABLO translocates to the nucleus and is colocalized with Survivin at mitotic spindles during apoptosis resulting from G2/M arrest due to docetaxel treatment of DU145 prostate cancer cells. Our data demonstrate that the nuclear interaction of Smac/DIABLO with Survivin is an important step for suppressing the anti-apoptotic function of Survivin in Doc-induced apoptosis. This suggests that the balance between cellular Smac/DIABLO and Survivin levels could be critical for cellular destiny in taxane-treated cancer cells.

AB - Smac/DIABLO is released by mitochondria in response to apoptotic stimuli and is thought to antagonize the function of inhibitors of apoptosis proteins. Recently, it has been shown that, like XIAP, Survivin can potentially interact with Smac/DIABLO. However, the precise mechanisms and cellular location of their action have not been determined. We report for the first time that Smac/DIABLO translocates to the nucleus and is colocalized with Survivin at mitotic spindles during apoptosis resulting from G2/M arrest due to docetaxel treatment of DU145 prostate cancer cells. Our data demonstrate that the nuclear interaction of Smac/DIABLO with Survivin is an important step for suppressing the anti-apoptotic function of Survivin in Doc-induced apoptosis. This suggests that the balance between cellular Smac/DIABLO and Survivin levels could be critical for cellular destiny in taxane-treated cancer cells.

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KW - G2/M arrest

KW - Mitotic apparatus

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KW - Smac

KW - Survivin

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Nuclear interaction of Smac/DIABLO with Survivin at G2/M arrest prompts docetaxel-induced apoptosis in DU145 prostate cancer cells

Abstract

Keywords

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