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Nuclear hormone receptor corepressor promotes esophageal cancer cell invasion by transcriptional repression of interferon-γ–inducible protein 10 in a casein kinase 2–dependent manner

Aberrant expression of casein kinase 2 (CK2) is associated with tumor progression; however, the molecular mechanism by which CK2 modulates tumorigenesis is incompletely understood. In this paper, we show that CK2α phosphorylates the C-terminal domain of the nuclear receptor corepressor (NCoR) at Ser...

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Autores principales: Yoo, Jung-Yoon, Choi, Hyo-Kyoung, Choi, Kyung-Chul, Park, Soo-Yeon, Ota, Ichiro, Yook, Jong In, Lee, Yoo-Hyun, Kim, Kunhong, Yoon, Ho-Geun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The American Society for Cell Biology 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408420/
https://www.ncbi.nlm.nih.gov/pubmed/22675025
http://dx.doi.org/10.1091/mbc.E11-11-0947
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author Yoo, Jung-Yoon
Choi, Hyo-Kyoung
Choi, Kyung-Chul
Park, Soo-Yeon
Ota, Ichiro
Yook, Jong In
Lee, Yoo-Hyun
Kim, Kunhong
Yoon, Ho-Geun
author_facet Yoo, Jung-Yoon
Choi, Hyo-Kyoung
Choi, Kyung-Chul
Park, Soo-Yeon
Ota, Ichiro
Yook, Jong In
Lee, Yoo-Hyun
Kim, Kunhong
Yoon, Ho-Geun
author_sort Yoo, Jung-Yoon
collection PubMed
description Aberrant expression of casein kinase 2 (CK2) is associated with tumor progression; however, the molecular mechanism by which CK2 modulates tumorigenesis is incompletely understood. In this paper, we show that CK2α phosphorylates the C-terminal domain of the nuclear receptor corepressor (NCoR) at Ser-2436 to stabilize the NCoR against the ubiquitin-dependent proteasomal degradation pathway. Importantly, NCoR promoted the invasion of esophageal cancer cells in a CK2-dependent manner. By using cyclic DNA microarray analysis, we identified CXCL10/IP-10 as a novel CK2α-NCoR cascade–regulated gene. The depletion of both NCoR and HDAC3 commonly derepressed IP-10 transcription, demonstrating the functional engagement of the NCoR-HDAC3 axis in IP-10 transcriptional repression. Furthermore, chromatin immunoprecipitation assays showed that c-Jun recruits NCoR-HDAC3 corepressor complexes to the (AP1 site of IP-10, leading to histone hypoacetylation and IP-10 down-regulation. Collectively these data suggest that the CK2α-NCoR cascade selectively represses the transcription of IP-10 and promotes oncogenic signaling in human esophageal cancer cells.
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spelling pubmed-34084202012-10-16 Nuclear hormone receptor corepressor promotes esophageal cancer cell invasion by transcriptional repression of interferon-γ–inducible protein 10 in a casein kinase 2–dependent manner Yoo, Jung-Yoon Choi, Hyo-Kyoung Choi, Kyung-Chul Park, Soo-Yeon Ota, Ichiro Yook, Jong In Lee, Yoo-Hyun Kim, Kunhong Yoon, Ho-Geun Mol Biol Cell Articles Aberrant expression of casein kinase 2 (CK2) is associated with tumor progression; however, the molecular mechanism by which CK2 modulates tumorigenesis is incompletely understood. In this paper, we show that CK2α phosphorylates the C-terminal domain of the nuclear receptor corepressor (NCoR) at Ser-2436 to stabilize the NCoR against the ubiquitin-dependent proteasomal degradation pathway. Importantly, NCoR promoted the invasion of esophageal cancer cells in a CK2-dependent manner. By using cyclic DNA microarray analysis, we identified CXCL10/IP-10 as a novel CK2α-NCoR cascade–regulated gene. The depletion of both NCoR and HDAC3 commonly derepressed IP-10 transcription, demonstrating the functional engagement of the NCoR-HDAC3 axis in IP-10 transcriptional repression. Furthermore, chromatin immunoprecipitation assays showed that c-Jun recruits NCoR-HDAC3 corepressor complexes to the (AP1 site of IP-10, leading to histone hypoacetylation and IP-10 down-regulation. Collectively these data suggest that the CK2α-NCoR cascade selectively represses the transcription of IP-10 and promotes oncogenic signaling in human esophageal cancer cells. The American Society for Cell Biology 2012-08-01 /pmc/articles/PMC3408420/ /pubmed/22675025 http://dx.doi.org/10.1091/mbc.E11-11-0947 Text en © 2012 Yoo et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0). “ASCB®,” “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society of Cell BD; are registered trademarks of The American Society of Cell Biology.
spellingShingle Articles
Yoo, Jung-Yoon
Choi, Hyo-Kyoung
Choi, Kyung-Chul
Park, Soo-Yeon
Ota, Ichiro
Yook, Jong In
Lee, Yoo-Hyun
Kim, Kunhong
Yoon, Ho-Geun
Nuclear hormone receptor corepressor promotes esophageal cancer cell invasion by transcriptional repression of interferon-γ–inducible protein 10 in a casein kinase 2–dependent manner
title Nuclear hormone receptor corepressor promotes esophageal cancer cell invasion by transcriptional repression of interferon-γ–inducible protein 10 in a casein kinase 2–dependent manner
title_full Nuclear hormone receptor corepressor promotes esophageal cancer cell invasion by transcriptional repression of interferon-γ–inducible protein 10 in a casein kinase 2–dependent manner
title_fullStr Nuclear hormone receptor corepressor promotes esophageal cancer cell invasion by transcriptional repression of interferon-γ–inducible protein 10 in a casein kinase 2–dependent manner
title_full_unstemmed Nuclear hormone receptor corepressor promotes esophageal cancer cell invasion by transcriptional repression of interferon-γ–inducible protein 10 in a casein kinase 2–dependent manner
title_short Nuclear hormone receptor corepressor promotes esophageal cancer cell invasion by transcriptional repression of interferon-γ–inducible protein 10 in a casein kinase 2–dependent manner
title_sort nuclear hormone receptor corepressor promotes esophageal cancer cell invasion by transcriptional repression of interferon-γ–inducible protein 10 in a casein kinase 2–dependent manner
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408420/
https://www.ncbi.nlm.nih.gov/pubmed/22675025
http://dx.doi.org/10.1091/mbc.E11-11-0947
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