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Tytuł:
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Nuclear β-catenin expression is positively regulated by JAB1 in human colorectal cancer cells.
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Autorzy:
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Nishimoto A; Department of Surgery and Clinical Science, Yamaguchi University Graduate School of Medicine, Ube, Japan; Department of Medical Education, Yamaguchi University Graduate School of Medicine, Ube, Japan. Electronic address: .
Takemoto Y; Department of Surgery and Clinical Science, Yamaguchi University Graduate School of Medicine, Ube, Japan.
Saito T; Department of Surgery and Clinical Science, Yamaguchi University Graduate School of Medicine, Ube, Japan.
Kurazumi H; Department of Surgery and Clinical Science, Yamaguchi University Graduate School of Medicine, Ube, Japan.
Tanaka T; Department of Surgery and Clinical Science, Yamaguchi University Graduate School of Medicine, Ube, Japan.
Harada E; Department of Surgery and Clinical Science, Yamaguchi University Graduate School of Medicine, Ube, Japan.
Shirasawa B; Department of Medical Education, Yamaguchi University Graduate School of Medicine, Ube, Japan.
Hamano K; Department of Surgery and Clinical Science, Yamaguchi University Graduate School of Medicine, Ube, Japan.
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Źródło:
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Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2020 Dec 10; Vol. 533 (3), pp. 548-552. Date of Electronic Publication: 2020 Sep 23.
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Typ publikacji:
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Journal Article; Research Support, Non-U.S. Gov't
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Język:
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English
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Imprint Name(s):
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Publication: <2002- >: San Diego, CA : Elsevier
Original Publication: New York, Academic Press.
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MeSH Terms:
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COP9 Signalosome Complex/*physiology
Colorectal Neoplasms/*metabolism
Intracellular Signaling Peptides and Proteins/*physiology
Peptide Hydrolases/*physiology
beta Catenin/*metabolism
Cell Line, Tumor ; Cell Nucleus/metabolism ; DNA Topoisomerases, Type II/metabolism ; Humans ; Ki-67 Antigen/metabolism ; Poly-ADP-Ribose Binding Proteins/metabolism ; Proto-Oncogene Proteins c-myc/metabolism ; Transcription Factor 7-Like 2 Protein/metabolism
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Contributed Indexing:
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Keywords: Colorectal cancer; JAB1; Nuclear β-catenin; c-MYC
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Substance Nomenclature:
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0 (CTNNB1 protein, human)
0 (Intracellular Signaling Peptides and Proteins)
0 (Ki-67 Antigen)
0 (MYC protein, human)
0 (Poly-ADP-Ribose Binding Proteins)
0 (Proto-Oncogene Proteins c-myc)
0 (Transcription Factor 7-Like 2 Protein)
0 (beta Catenin)
EC 3.4.- (Peptide Hydrolases)
EC 3.4.-.- (COPS5 protein, human)
EC 3.4.19.12 (COP9 Signalosome Complex)
EC 5.99.1.3 (DNA Topoisomerases, Type II)
EC 5.99.1.3 (TOP2A protein, human)
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Entry Date(s):
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Date Created: 20200926 Date Completed: 20210315 Latest Revision: 20210315
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Update Code:
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20240105
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DOI:
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10.1016/j.bbrc.2020.09.007
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PMID:
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32977947
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Wnt/β-catenin signaling is important for development and progression of colorectal cancer (CRC). The degradation complex for β-catenin is functionally impaired in CRC cells, thereby resulting in the accumulation of β-catenin and its translocation into the nucleus. Nuclear β-catenin interacts with and co-activates T cell factor4 (TCF4), resulting in β-catenin/TCF4-dependent transcription. Therefore, nuclear β-catenin has been categorized as the main driving force in the tumorigenesis of CRC. Recent studies reveal that Jun activation domain-binding protein 1 (JAB1) enhances the degradation of seven in absentia homolog-1 (SIAH-1), a putative E3 ubiquitin ligase of β-catenin, and positively regulates the expression of total β-catenin in human CRC cells. An another recent study also shows that nuclear β-catenin is ubiquitinated and degraded by an E3 ubiquitin ligase, tripartite motif-containing protein 33 (TRIM33). However, the regulatory mechanism for the expression of nuclear β-catenin remains to be fully understood. In this study, we have demonstrated that JAB1 positively regulates the expression of nuclear β-catenin, c-MYC as a β-catenin/TCF4 target, and cell cycle regulators, such as Ki-67 and topoisomerase IIα, in human CRC cells. Taken together, these results suggest that JAB1 is considered as a promising target for novel CRC therapy.
Competing Interests: Declaration of competing interest The authors declare no conflicts of interest.
(Copyright © 2020. Published by Elsevier Inc.)