Interaction of SOCS3 with NonO attenuates IL-1β-dependent MUC8 gene expression

Kyoung Seob Song; Kyubo Kim; Kwang Chul Chung; Jae Hong Seol; Joo Heon Yoon

doi:10.1016/j.bbrc.2008.10.084

Interaction of SOCS3 with NonO attenuates IL-1β-dependent MUC8 gene expression

Kyoung Seob Song, Kyubo Kim, Kwang Chul Chung, Jae Hong Seol, Joo Heon Yoon

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

17 Citations (Scopus)

Abstract

The intracellular negatively regulatory mechanism which affects IL-1β-induced MUC8 gene expression remains unclear. We found that SOCS3 overexpression suppressed IL-1β-induced MUC8 gene expression in NCI-H292 cells, whereas silencing of SOCS3 restored IL-1β-induced MUC8 gene expression. Sequentially activated ERK1/2, RSK1, and CREB by IL-1β were not affected by SOCS3, indicating that SOCS3 has an independent mechanism of action. Using immunoprecipitaion and nano LC mass analysis, we found that SOCS3 bound NonO (non-POU-domain containing, octamer-binding domain protein) in the absence of IL-1β, whereas IL-1β treatment dissociated the direct binding of SOCS3 and NonO. A dominant-negative SOCS3 mutant (Y204F/Y221F) did not bind to NonO. Interestingly, SOCS3 overexpression dramatically suppressed MUC8 gene expression in cells transfected with wild-type or siRNA of NonO. Moreover, silencing of SOCS3 dramatically increased NonO-mediated MUC8 gene expression caused by IL-1β compared to NonO overexpression alone, suggesting that SOCS3 acts as a suppressor by regulating the action of NonO.

Original language	English
Pages (from-to)	946-951
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	377
Issue number	3
DOIs	https://doi.org/10.1016/j.bbrc.2008.10.084
Publication status	Published - 2008 Dec 19

Bibliographical note

Funding Information:
This study was supported by a Korean Science and Engineering Foundation (KOSEF) grant funded by the Korea government (MOST) (R11-2007-040-02001-0 for JHY), by Korea Research Foundation Grant KRF-2005-050-C00005 (for KSS), and by a faculty research grant of Yonsei University College of Medicine for 2007 (6-2007-0178 for KSS). The authors have no conflicting financial interests.

All Science Journal Classification (ASJC) codes

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1016/j.bbrc.2008.10.084

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title = "Interaction of SOCS3 with NonO attenuates IL-1β-dependent MUC8 gene expression",

abstract = "The intracellular negatively regulatory mechanism which affects IL-1β-induced MUC8 gene expression remains unclear. We found that SOCS3 overexpression suppressed IL-1β-induced MUC8 gene expression in NCI-H292 cells, whereas silencing of SOCS3 restored IL-1β-induced MUC8 gene expression. Sequentially activated ERK1/2, RSK1, and CREB by IL-1β were not affected by SOCS3, indicating that SOCS3 has an independent mechanism of action. Using immunoprecipitaion and nano LC mass analysis, we found that SOCS3 bound NonO (non-POU-domain containing, octamer-binding domain protein) in the absence of IL-1β, whereas IL-1β treatment dissociated the direct binding of SOCS3 and NonO. A dominant-negative SOCS3 mutant (Y204F/Y221F) did not bind to NonO. Interestingly, SOCS3 overexpression dramatically suppressed MUC8 gene expression in cells transfected with wild-type or siRNA of NonO. Moreover, silencing of SOCS3 dramatically increased NonO-mediated MUC8 gene expression caused by IL-1β compared to NonO overexpression alone, suggesting that SOCS3 acts as a suppressor by regulating the action of NonO.",

author = "Song, {Kyoung Seob} and Kyubo Kim and Chung, {Kwang Chul} and Seol, {Jae Hong} and Yoon, {Joo Heon}",

note = "Funding Information: This study was supported by a Korean Science and Engineering Foundation (KOSEF) grant funded by the Korea government (MOST) (R11-2007-040-02001-0 for JHY), by Korea Research Foundation Grant KRF-2005-050-C00005 (for KSS), and by a faculty research grant of Yonsei University College of Medicine for 2007 (6-2007-0178 for KSS). The authors have no conflicting financial interests.",

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doi = "10.1016/j.bbrc.2008.10.084",

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AU - Kim, Kyubo

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AU - Seol, Jae Hong

AU - Yoon, Joo Heon

N1 - Funding Information: This study was supported by a Korean Science and Engineering Foundation (KOSEF) grant funded by the Korea government (MOST) (R11-2007-040-02001-0 for JHY), by Korea Research Foundation Grant KRF-2005-050-C00005 (for KSS), and by a faculty research grant of Yonsei University College of Medicine for 2007 (6-2007-0178 for KSS). The authors have no conflicting financial interests.

PY - 2008/12/19

Y1 - 2008/12/19

N2 - The intracellular negatively regulatory mechanism which affects IL-1β-induced MUC8 gene expression remains unclear. We found that SOCS3 overexpression suppressed IL-1β-induced MUC8 gene expression in NCI-H292 cells, whereas silencing of SOCS3 restored IL-1β-induced MUC8 gene expression. Sequentially activated ERK1/2, RSK1, and CREB by IL-1β were not affected by SOCS3, indicating that SOCS3 has an independent mechanism of action. Using immunoprecipitaion and nano LC mass analysis, we found that SOCS3 bound NonO (non-POU-domain containing, octamer-binding domain protein) in the absence of IL-1β, whereas IL-1β treatment dissociated the direct binding of SOCS3 and NonO. A dominant-negative SOCS3 mutant (Y204F/Y221F) did not bind to NonO. Interestingly, SOCS3 overexpression dramatically suppressed MUC8 gene expression in cells transfected with wild-type or siRNA of NonO. Moreover, silencing of SOCS3 dramatically increased NonO-mediated MUC8 gene expression caused by IL-1β compared to NonO overexpression alone, suggesting that SOCS3 acts as a suppressor by regulating the action of NonO.

AB - The intracellular negatively regulatory mechanism which affects IL-1β-induced MUC8 gene expression remains unclear. We found that SOCS3 overexpression suppressed IL-1β-induced MUC8 gene expression in NCI-H292 cells, whereas silencing of SOCS3 restored IL-1β-induced MUC8 gene expression. Sequentially activated ERK1/2, RSK1, and CREB by IL-1β were not affected by SOCS3, indicating that SOCS3 has an independent mechanism of action. Using immunoprecipitaion and nano LC mass analysis, we found that SOCS3 bound NonO (non-POU-domain containing, octamer-binding domain protein) in the absence of IL-1β, whereas IL-1β treatment dissociated the direct binding of SOCS3 and NonO. A dominant-negative SOCS3 mutant (Y204F/Y221F) did not bind to NonO. Interestingly, SOCS3 overexpression dramatically suppressed MUC8 gene expression in cells transfected with wild-type or siRNA of NonO. Moreover, silencing of SOCS3 dramatically increased NonO-mediated MUC8 gene expression caused by IL-1β compared to NonO overexpression alone, suggesting that SOCS3 acts as a suppressor by regulating the action of NonO.

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Interaction of SOCS3 with NonO attenuates IL-1β-dependent MUC8 gene expression

Abstract

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