p34sei-1 inhibits ros-induced cell death through suppression of ASK1

Seung Woo Hong; Jae Sik Shin; Young Min Lee; Dong Gil Kim; Sok Young Lee; Dok Hyun Yoon; Seong Yun Jung; Jung Jin Hwang; Seung Jin Lee; Dong Hyung Cho; Yong Sang Hong; Tae Won Kim; Dong Hoon Jin; Won Keun Lee

doi:10.4161/cbt.12.5.15972

p34sei-1 inhibits ros-induced cell death through suppression of ASK1

Seung Woo Hong, Jae Sik Shin, Young Min Lee, Dong Gil Kim, Sok Young Lee, Dok Hyun Yoon, Seong Yun Jung, Jung Jin Hwang, Seung Jin Lee, Dong Hyung Cho, Yong Sang Hong, Tae Won Kim, Dong Hoon Jin, Won Keun Lee

Pediatric Blood & Marrow Transplant & Cellular Therapy

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

20 Scopus citations

Abstract

Apoptosis signal-regulating kinase 1 (ASK1) is a key factor for controlling several cellular events including the cell cycle senescence and apoptosis in response to reactive oxygen species (ROS). However the mechanisms that regulate ASK1 protein levels remain largely unexplored. In this study we demonstrate that p34^SEI-1 a positive cell cycle regulator with an oncogenic potential inhibits ROS-induced cell death by suppressing ASK1. We first found that p34^SEI-1-expressing cells have enhanced resistance to hydrogen peroxide (H₂O₂). Moreover ectopic expression of p34 ^SEI-1 clearly inhibited H₂O₂- induced phosphorylation of ASK1 in the colon cancer cell lines-HCT116 and SW620-in association with a decrease in ASK1 protein levels. Interestingly p34 ^SEI-1 induced ubiquitination of ASK1 however no direct interaction was found between p34^SEI-1 and ASK1. These results suggest that p34SEI-1 inhibits ROS-induced cell death through by indirectly inducing ubiquitination of ASK1.

Original language	English (US)
Pages (from-to)	421-426
Number of pages	6
Journal	Cancer Biology and Therapy
Volume	12
Issue number	5
DOIs	https://doi.org/10.4161/cbt.12.5.15972
State	Published - Sep 1 2011

Bibliographical note

Funding Information:
This study was supported by grants from the Korea Health 21 R&D Project, Ministry of Health and Welfare and Family Affairs, Republic of Korea (A062254), and the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (20100015972).

Keywords

ASK1
ROS
Ubiquitination
p34SEI-1

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.4161/cbt.12.5.15972

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title = "p34sei-1 inhibits ros-induced cell death through suppression of ASK1",

abstract = "Apoptosis signal-regulating kinase 1 (ASK1) is a key factor for controlling several cellular events including the cell cycle senescence and apoptosis in response to reactive oxygen species (ROS). However the mechanisms that regulate ASK1 protein levels remain largely unexplored. In this study we demonstrate that p34SEI-1 a positive cell cycle regulator with an oncogenic potential inhibits ROS-induced cell death by suppressing ASK1. We first found that p34SEI-1-expressing cells have enhanced resistance to hydrogen peroxide (H2O2). Moreover ectopic expression of p34 SEI-1 clearly inhibited H2O2- induced phosphorylation of ASK1 in the colon cancer cell lines-HCT116 and SW620-in association with a decrease in ASK1 protein levels. Interestingly p34 SEI-1 induced ubiquitination of ASK1 however no direct interaction was found between p34SEI-1 and ASK1. These results suggest that p34SEI-1 inhibits ROS-induced cell death through by indirectly inducing ubiquitination of ASK1.",

keywords = "ASK1, ROS, Ubiquitination, p34SEI-1",

author = "Hong, {Seung Woo} and Shin, {Jae Sik} and Lee, {Young Min} and Kim, {Dong Gil} and Lee, {Sok Young} and Yoon, {Dok Hyun} and Jung, {Seong Yun} and Hwang, {Jung Jin} and Lee, {Seung Jin} and Cho, {Dong Hyung} and Hong, {Yong Sang} and Kim, {Tae Won} and Jin, {Dong Hoon} and Lee, {Won Keun}",

note = "Funding Information: This study was supported by grants from the Korea Health 21 R&D Project, Ministry of Health and Welfare and Family Affairs, Republic of Korea (A062254), and the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (20100015972).",

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doi = "10.4161/cbt.12.5.15972",

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AU - Hong, Seung Woo

AU - Shin, Jae Sik

AU - Lee, Young Min

AU - Kim, Dong Gil

AU - Lee, Sok Young

AU - Yoon, Dok Hyun

AU - Jung, Seong Yun

AU - Hwang, Jung Jin

AU - Lee, Seung Jin

AU - Cho, Dong Hyung

AU - Hong, Yong Sang

AU - Kim, Tae Won

AU - Jin, Dong Hoon

AU - Lee, Won Keun

N1 - Funding Information: This study was supported by grants from the Korea Health 21 R&D Project, Ministry of Health and Welfare and Family Affairs, Republic of Korea (A062254), and the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (20100015972).

PY - 2011/9/1

Y1 - 2011/9/1

N2 - Apoptosis signal-regulating kinase 1 (ASK1) is a key factor for controlling several cellular events including the cell cycle senescence and apoptosis in response to reactive oxygen species (ROS). However the mechanisms that regulate ASK1 protein levels remain largely unexplored. In this study we demonstrate that p34SEI-1 a positive cell cycle regulator with an oncogenic potential inhibits ROS-induced cell death by suppressing ASK1. We first found that p34SEI-1-expressing cells have enhanced resistance to hydrogen peroxide (H2O2). Moreover ectopic expression of p34 SEI-1 clearly inhibited H2O2- induced phosphorylation of ASK1 in the colon cancer cell lines-HCT116 and SW620-in association with a decrease in ASK1 protein levels. Interestingly p34 SEI-1 induced ubiquitination of ASK1 however no direct interaction was found between p34SEI-1 and ASK1. These results suggest that p34SEI-1 inhibits ROS-induced cell death through by indirectly inducing ubiquitination of ASK1.

AB - Apoptosis signal-regulating kinase 1 (ASK1) is a key factor for controlling several cellular events including the cell cycle senescence and apoptosis in response to reactive oxygen species (ROS). However the mechanisms that regulate ASK1 protein levels remain largely unexplored. In this study we demonstrate that p34SEI-1 a positive cell cycle regulator with an oncogenic potential inhibits ROS-induced cell death by suppressing ASK1. We first found that p34SEI-1-expressing cells have enhanced resistance to hydrogen peroxide (H2O2). Moreover ectopic expression of p34 SEI-1 clearly inhibited H2O2- induced phosphorylation of ASK1 in the colon cancer cell lines-HCT116 and SW620-in association with a decrease in ASK1 protein levels. Interestingly p34 SEI-1 induced ubiquitination of ASK1 however no direct interaction was found between p34SEI-1 and ASK1. These results suggest that p34SEI-1 inhibits ROS-induced cell death through by indirectly inducing ubiquitination of ASK1.

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KW - Ubiquitination

KW - p34SEI-1

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p34sei-1 inhibits ros-induced cell death through suppression of ASK1

Abstract

Bibliographical note

Keywords

UN SDGs

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